Histopathological Alterations Research Articles

The Effect of Boric Acid on Oxidative Stress, Inflammation, and Apoptosis in Embryonic and Fetal Tissues Damage Caused by Consumption of High-Fructose Corn Syrup in Pregnant Rats

Abstract This study aimed to determine the protective role of boric acid in a pregnant rat model of high fructose corn syrup consumption. Consumption of high fructose corn syrup has been associated with adverse health outcomes in humans and animals. Twenty-eight healthy female Wistar albino rats (250–300 g weight and 16–24 weeks old) were randomly distributed into four equal groups (n = 7): Control, Boric acid (BA), High Fructose Corn Syrup (HFCS), HFCS + BA. Boric acid (20 mg/kg) was administered to pregnant rats via oral gavage every day during pregnancy. The prepared 30% HFCS (F30) solution (24% fructose, 28% dextrose) was added to the drinking water throughout pregnancy. At the end of pregnancy (day 19), blood, placenta, uterus, and fetuses were collected from rats. The results indicated that HFCS increases oxidative stress by increasing the level of MDA and decreasing GSH, SOD, and CAT activity in the blood of maternal. However, BA administration significantly decreased MDA levels and increased GSH levels, SOD, and CAT activity (p < 0.05). In addition, HFCS consumption significantly increased plasma TNF-α, IL-6, and leptin levels compared to control, BA, and HFCS + BA groups (p < 0.05). However, BA administration significantly decreased plasma TNF-α, IL-6, and leptin levels (p < 0.05). Furthermore, BA (20 mg/kg) significantly decreased HFCS-induced histopathological and immunohistochemical alterations in the placenta, uterus, and fetal tissue. In conclusion, BA may prevent HFCS toxicity in maternal and fetal tissues, as it regulates oxidative imbalance in pregnant rat and alleviates histopathological and immunohistochemical changes. The findings indicate a need for further studies to assess the potential of boron in preventing or mitigating the effects of HFCS during pregnancy. Graphical Abstract

Replacement of fishmeal with Quinoa Husk (Chenopodium quinoa) for mitigating multiple stresses in Pangasianodon Hypophthalmus

The fishmeal is boon for aquaculture production in this recent pollution and climate change era. However, the demand of fishmeal is enhancing in many folds which needs to find alternative to fishmeal in cheap price. The present investigation addresses these issues with quinoa husk (QH). An experiment was performed to evaluate replacement of fishmeal by QH in different proportionate at 0, 15, 20, 25, 30 and 35%. The study was designed with 12 treatments as control, stressors group (concurrent exposed to ammonia, arsenic and high temperature stress, NH3+As+T), group fed with QH at 15, 20, 25, 30 and 35% without and with stressors (NH3+As+T) in Pangasianodon hypophthalmus for 105 days. The optimization of QH dose for growth performance such as food conversion ratio, growth rate, protein efficiency ratio and specific growth rate with respect to protein percentage and obtained 26%. The oxidative enzymes such as superoxide dismutase (SOD), catalase (CAT), glutathione-s-transferase (GST) and glutathione peroxidase (GPx) in gill, kidney and liver tissues were significantly lowered by replacement of fishmeal by QH at 25% in fish reared under arsenic and ammonia toxicity and high temperature stress (NH3+As+T). The neurotransmitter enzyme (AChE) in brain tissue was noticeably enhanced by QH at 25%. The aspartate amino transferase (AST) and alanine amino transferase (ALT) as well as malate dehydrogenase (MDH) and lactate dehydrogenase (LDH) in gill and liver were significantly reduced by QH at 25% in fish reread under multiple stresses (NH3+As+T). The nitro blue tetrazolium (NBT), blood glucose, albumin, globulin, total protein, A:G ratio, myeloperoxidase (MPO) and total immunoglobulin (Ig) were noticeably improved by supplementation of QH at 25–30% in fish reared under NH3+As+T. The amylase, protease and lipase were significant improved with replacement of fishmeal by QH at 25%. The histo-pathological alterations were marked in liver and gill tissues, whereas these tissues were protected by QH at 25% in fish reared under control and stress condition (NH3+As+T). The present study revealed that replacement of fishmeal at 25% by QH could be a better replacement for improvement in anti-oxidative status, acetylcholine esterase and growth performance in fish reread under NH3+As+T stress.

Protective Effect of Flaxseed Oil on Diazinon-Induced Cardiotoxicity in Rats in Sub-Chronic Exposure

Background: Diazinon (DZN), an organophosphate insecticide, exerts various adverse effects on human organs. In this study, we investigated the potential cardiotoxic effects of flaxseed oil (FS oil) on oxidative stress caused by DZN in the heart tissue of rats. Methods: Thirty male rats were divided into five groups: a control group receiving normal saline, an FS oil group administered 200 mg/kg/d of FS oil, a DZN group treated with 70 mg/kg/d of DZN, and two co-treatment groups receiving DZN alongside FS oil at 100 and 200 mg/kg/d. We assessed oxidative stress biomarkers in heart tissue, including malondialdehyde, total oxidant status, catalase, superoxide dismutase, and total thiol content. Heart tissue morphology was analyzed using hematoxylin and eosin staining. Results: DZN significantly increased the levels of malondialdehyde (12.04±1.16) and total oxidant status (0.43±0.01) and also decreased the content of catalase (23.09±1.99), superoxide dismutase (5.52±0.61), and total thiol content (6.31±0.77) in heart tissue. FS-oil + DZN decreased malondialdehyde (10.88±0.31) and total oxidant status (0.41±0.01) and also increased the content of catalase (29.34±1.77), superoxide dismutase (6.64±0.21), and total thiol content (8.20±0.15) in heart tissue. FS oil supplement consumption reversed oxidative stress status in a dose-dependent manner. Furthermore, FS oil ameliorated heart histopathological alterations induced by DZN. Conclusion: Our findings confirmed that DZN induced heart toxicity and that FS oil had protective effects. Additionally, FS oil supplementation conferred protective effects on the heart against toxicity induced by DZN.

Abatement by Alhagi maurorum of lead-induced nephrotoxicity in rats: emphasis on Nrf2/HO-1

BackgroundLead (Pb) is a heavy metal with extreme toxicity and numerous industrial uses. It produces nephrotoxicity with notable changes in renal architecture and function. The Alhagi maurorum (AM) belongs to the family Fabaceae and is native to the Middle East area. In the present study, the potential nephroprotective effects of AM in Pb-intoxicated rats were evaluated.ResultsAM methanolic extract was standardized in reference to its main phenolic compounds orientin, rutin, and quercetin. Acute oral toxicity studies indicated that the extract is safe for animals. Rats were allocated into five groups and treated for 28 days as follows: control, AM (200 mg/kg, orally), Pb (15 mg/kg, orally), Pb + AM (100 mg/kg), and Pb + AM (200 mg/kg). Pb administration markedly increased serum cystatin C, urea, creatinine levels, and urinary NAG. Pb also caused renal histopathological alterations. However, AM o-treatment ameliorated such pathological changes. In addition, AM treatment prevented Pb-induced accumulation of malondialdehyde (MDA), attenuated glutathione (GSH) depletion, and catalase (CAT) and superoxide dismutase (SOD) exhaustion. AM guarded against Pb-induced enhanced the protein expression of interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α), cyclooxygenase-2 (COX-2), and nuclear factor-kappa B (NF-κB). Further, AM significantly prevented Pb-induced upregulation of mRNA levels of Bax and downregulation of Bcl-2. These effects were associated with increased levels of heme oxygenase-1 (HO-1) and nuclear factor erythroid 2-related factor 2 (Nrf2) in renal tissue.ConclusionAM guards against Pb-induced nephrotoxicity in rats that involve, at least partly, the antioxidant, anti-inflammatory, and anti-apoptotic activities as well as the modulation of HO-1 and Nrf2 expression.

Study on the Role and Pathological and Immune Responses of Silver Nanoparticles Against Two Aeromonas salmonicida subsp. salmonicida Strains at Different Virulence Levels in Rainbow Trout (Oncorhynchus mykiss)

Aeromonas species are among the main pathogens causing rainbow trout infections. Silver nanoparticles (AgNPs) have a broad spectrum of antimicrobial properties and are usually produced by various green-synthesis methods. However, the application of commercialized AgNPs has not fully been clarified. Thus, the objective of this study was to evaluate the antibacterial activities of commercialized AgNPs (range of sizes 10–12 nm) on two contrasting A. salmonicida strains (I-1 and I-4), isolated from rainbow trout; the antibacterial mechanism, histopathological alterations and the expression of immune-related genes were investigated. In vitro, the minimal inhibitory concentration (MIC) was 10 µg/mL for I-1, and lowered to 9.5 µg/mL for I-4, respectively. AgNPs were shown to disrupt both the cell wall and membrane of I-1 and I-4, resulting in cell lysis and degradation. In vivo, rainbow trout challenged by immersed or intraperitoneally injected infection, the 10 µg/mL AgNP-treated groups, both showed delayed deaths and lower mortalities compared to the control groups, without any clinical signs and pathological changes. Especially for the virulent I-4, the enhanced expressions of immune-related genes TNF-α, IL-1β, IL-10 and IL-11 were significantly reduced in the AgNP-treated group, indicating a lesser inflammation due to the application of AgNPs. This study would lay theoretical foundation for the wide application of silver nanoparticles in fish diseases.

Salinity modulation of neodymium and dysprosium toxicity in mussels: A comprehensive analysis of adult and sperm responses.

Neodymium (Nd) and dysprosium (Dy) are among the most commonly used rare earth elements (REEs) worldwide, leading to their increased concentrations in aquatic environments, with potential impacts on organisms. Additionally, organisms are also subjected to environmental stressors, such as salinity shifts, which can not only directly impact their health but also modulate the impacts of contaminants. Therefore, this study aimed to evaluate the effects of Nd and Dy on adult mussels and sperm of the species Mytilus galloprovincialis after 28days and 30min of exposure, respectively. Furthermore, the study assessed how salinity shifts influence the effects of these elements. To this end, histopathological and biochemical alterations were evaluated in adults, while biochemical and physiological changes were analyzed in sperm. To simplify data interpretation and understand the overall impact of each treatment, Multidimensional Scaling Analysis (MDS) and the Integrated Biological Index (IBR) were used. The MDS analysis identified three groups that were consistent with the IBR score. The first group, composed of the treatments at a salinity of 40, showed medium to severe effects. The second group was comprised of the treatments at control salinity (30), which presented the lowest IBR scores, indicating the least impact. The third group, which included the treatments at a salinity of 20, was associated with the most severe impacts, with Dy and Nd presenting the highest IBR scores. The results showed that salinity was the most predominant factor in this study, with the lower salinity being the most harmful. In addition, within each salinity level, Dy was the element that induced the highest response in this species. This study provides valuable information regarding the impacts of the interaction between REEs and salinity shifts, highlighting the importance of such research in mitigating the effects of pollution and climate change on marine ecosystems.

Therapeutic Efficacy of Lavandula dentata’s Oil and Ethanol Extract in Regulation of the Neuroinflammation, Histopathological Alterations, Oxidative Stress, and Restoring Balance Treg Cells Expressing FoxP3+ in a Rat Model of Epilepsy

Background/Objectives: Despite the availability of antiepileptic drugs (AEDs) that can manage seizures, they often come with cognitive side effects. Furthermore, the role of oxidative stress and neuroinflammatory responses in epilepsy and the limitations of current AEDs necessitate exploring alternative therapeutic options. Medicinal plants, e.g., Lavandula dentata L., are rich in phenolic compounds and may provide neuroprotective and anti-inflammatory benefits. However, limited research evaluates their effectiveness in modulating neuroinflammation and histopathological changes in epilepsy models. Therefore, the current study hypothesized that treating Lavandula dentata L. extract or essential oils may reduce neuroinflammatory responses and mitigate histopathological changes in the brain, providing a natural alternative or adjunct therapy for epilepsy management. Methods: Five groups of male Wistar rats were used: control, pilocarpine-treated epileptic, valproic acid (VPA-treated epileptic), L. dentata extract, and essential oils. Numerous electrolyte levels, monoamine levels, neurotransmitter levels, and the mRNA expression of specific gate channel subtypes were evaluated in homogenate brain tissue. Additionally, histological changes in various brain regions were investigated. Results: The investigation revealed that the extract and essential oils obtained from L. dentata L. exhibited the ability to improve the modulation of electrolytes and ions across voltage- and ligand-gated ion channels. Furthermore, it was revealed that they could decrease neuronal excitability by facilitating repolarization. Moreover, L. dentata’s oil and ethanol extract re-balances T-reg/Th-17 cytokines, restoring the pro/anti-inflammatory cytokines and Treg markers, e.g., FOXP3 and CTLA-4, to their normal level. Conclusions: The present work confirms that the extract and essential oils of L. dentata L. have different activities to ameliorate the progression of histopathological alterations. Therefore, when used in conjunction with other AEDs, the extract and essential oils of L. dentata can slow the progression of epileptogenesis.

Comparative evaluation of the adverse effects wastewater effluents on Channa punctata through oxidative stress and histopathological alterations

This study investigates the adverse effects of wastewater effluents on Channa punctata, collected from upstream (Methwasa), point-source (Juna Nagda), and downstream (Parmarkheri) locations along the Chambal River at Nagda, Ujjain, India. The research focuses on oxidative stress responses and histopathological alterations in fish gills, liver, and kidneys. Catalase and glutathione S-transferase activities were significantly higher at Juna Nagda and Parmarkheri compared to the upstream site (Methwasa) (p < 0.05), suggesting the activation of antioxidant defense mechanisms due to pollution exposure. Histological analysis revealed the most severe tissue damage in fish from Juna Nagda, followed by Parmarkheri and Methwasa. The Integrated Biomarker Response (IBR) for oxidative stress and histopathological changes consistently indicated higher values at the polluted sites. Water temperature, electrical conductivity (EC), and nitrate levels were identified as potential factors influencing these biomarker responses. The study concludes that thermal effluents discharged into Juna Nagda are responsible for the observed effects. Overall, integrated biomarkers, particularly histopathological alterations, offer a reliable tool for monitoring the prolonged impacts of wastewater effluents on aquatic organisms.

Histopathological alteration in Zebrafish: Unravelling the Effects of Long-Term Copper Oxide Nanoparticle Exposure

Copper Oxide nanoparticles (CuO-NPs) are widely used and they build up in the aquatic environment and can be harmful to aquatic life. Aquatic creatures are affected by CuO NPs, yet the consequences of these particles have not been well explored despite contentious toxicological results. Therefore, this study aimed to investigate the effects of chronic exposure to CuO-NPs on adult zebrafish. The study was carried out by conducting physicochemical characterization of commercially procured CuO-NPs using UV/Vis, ICP-OES spectroscopy, Transmission Electron Microscopy (TEM), X-ray diffraction (XRD), and Fourier Transform Infrared Spectroscopy(FTIR). Following characterization, adult zebrafish were chronically exposed to 0.5, 1, and 3 mg/l of CuO-NPs. Characterization revealed a heterogeneous population of nanoparticles in the size ranges of 10–50 nm. Oxidative stress indicators and functional markers were studied in addition to tissue histology. Chronic exposure to adult Fish at concentrations of 1 and 3 mg/l exhibited increased levels of stress compared to lower concentrations of 0.5 mg/l. Observations from histology showed that the extent of tissue damage and injuries increased with the concentration of CuO-NPs. In conclusion, chronic exposure to ≤50nm-sized CuO-NPs exhibited toxic repercussions in adult zebrafish.

Integration of responses to lithium in mussels at different levels of biological complexity.

The increasing use of lithium (Li) in modern technology and medicine has raised up concerns in the scientific community due to the potential impact of this metal on the aquatic environment. Although several effects have been reported in different organisms, there is still scarce information concerning the mechanisms and chronic effects of Li toxicity in marine life. Our main objective is to determine biological effects of sub-lethal concentrations in Mytilus galloprovincialis at different biological organization levels using the biomarker approach. Mussels were exposed to environmental Li concentrations: 0.1, 1 and 10 mg/L. Samples of gills, muscle and digestive gland were taken at days 1, 7 and 21 for the assessment of biochemical, histochemical and histological endpoints. Results showed that exposure to Li caused greater impacts in a dose and time-dependent manner at different biological organization levels. Changes in acetylcholinesterase (AChE) activity were detected at day 1 (induction) and day 21 (inhibition) in accordance with increasing Li levels, indicating possible neurotoxic effects, while catalase (CAT) inhibition, and subsequent induction, was detected at day 1 in proportion to Li concentrations. Lysosomal biomarkers demonstrated a decreasing lysosomal membrane stability with higher Li doses after 21 days of exposure, whereas 10 mg Li/L provoked lysosomal size reduction from day 1. Finally, the integration of these biological responses into an IBR index indicated a clear effect of exposure after 21 days in a dose-dependent way, leading to cellular and tissue damage as consequence. Moreover, a time-course response was observed with an enhanced oxidative stress at day 1, and a neurotoxic effect, lysosomal membrane destabilization and histopathological alterations after 7 and 21 days of exposure to medium and high Li concentrations. Consequently, these findings provide valuable insights into Li's effects on marine life, emphasizing the need for further long-term studies across different biological organization levels.

Studies on ameliorative potentials of quercetin nanoparticles against imidacloprid induced subacute genotoxicity and histopathological alteration in Swiss albino mice

ABSTRACT Objective Genotoxicity assays include micronucleus test, comet assay, and malformed sperm head used to investigate the protective potential of quercetin and quercetin nanoparticles against imidacloprid-induced genotoxicity in Swiss albino mice. Method The ionic gelation procedure was used to synthesize the quercetin nanoparticles and characterized for their hydrodynamic diameter, zeta potential, SEM, TEM, FT-IR, and encapsulation efficiency. Total 48 mice were taken in eight groups with six animals in each group. Group 1, 2, 3 and 4 received 3% gum acacia, 22 mg/kg imidacloprid (IMI), 25 mg/kg quercetin (Que) and 25 mg/kg quercetin nanoparticles high dose [QNPs (HD)], respectively. Group 5, 6, 7 and 8 received 22 mg/kg imidacloprid + 25 mg/kg quercetin (IMI + Que), 22 mg/kg imidaclopid + 25 mg/kg quercetin nanoparticles [IMI + QNPs (HD)], 22 mg/kg imidacloprid + 12.5 mg/kg quercetin nanoparticle medium dose [IMI + QNPs (MD)] and 22 mg/kg imidacloprid + 6.25 mg/kg quercetin nanoparticles low dose [IMI + QNPs (LD)], respectively. Result The imidacloprid causes genotoxicity in bone marrow cells by increasing the frequency of micronuclei and the comet tail length. Additionally, imidacloprid is mutagenic to germ cells, as determined by a test for aberrant sperm heads. Both quercetin and quercetin nanoparticles lessen the genotoxicity that imidacloprid induces when administered together or separately. Histopathological findings also revealed degenerative changes in bone marrow and testes in imidacloprid administered group as compared to control. Conclusion Quercetin and quercetin nanoparticles showed marked ameliorative effect by restoring the degenerative changes produced by imidacloprid.

Impact of gamma-aminobutyric acid receptors modulators on renal and liver functional, molecular and histological characteristics in white male mice

The gamma-aminobutyric acid (GABA) receptors are considered the main receptors that inhibit neurotransmitters in the mammalian brain, and they have been proven to exist in non-neuronal cells. The study's purpose is to determine the impact of GABA modulation on renal and liver functions and molecular and histological characteristics using different doses of lorazepam. Lorazepam, one of the benzodiazepine drugs known for its modulatory effect on GABA receptors, has been used as a modulator to determine the impact of GABA modulation on renal and liver functions and molecular and histological characteristics in 30 albino male mice, out of which 21 were divided into 3 groups. Each group were treated with different dose of lorazepam (1 mg/kg, 2 mg/kg and 3 mg/kg body weight respectively). The rest 9 of animals were considered as a control group. Histological and functional parameters were studied in kidney and liver functional states to evaluate the impact of GAPA modulation using lorazepam. Total genomic DNA was extracted from liver, brain, kidney and blood and random amplification polymorphic DNA (RAPD) technique were used to detect the molecular impact of GABA modulation on the genomic DNA. The data were analyzed using SPSS Version 20.0 (SPSS Inc.), with means and standard deviations (SD) calculated for quantitative variables, and ANOVA applied for comparing group means. Functional parameters (blood urea, creatinine, GOT, GPT, GGT) and histopathological examination showed a significant change in treated groups compared to the control group. In both the liver and kidneys of mice, with increasing doses of lorazepam, there was an increase in the severity of congestive phenomena in blood vessels with the appearance of hemorrhages, signs of inflammation, and cell degeneration and necrosis. The molecular investigation indicated substantial changes in RAPD profiles of treated groups, with normal bands disappearing and novel bands appearing in contrast to the control group. The RAPD profiles of the treated and control samples revealed 432 bands, with 109 as control bands, 167 (loss of normal bands and emergence of novel bands) as polymorphic bands, and 156 as homomorphic bands. It is concluded that GABA modulation by lorazepam increases the functional and histopathological alterations, producing variations in the genomic DNA.

Mangiferin mitigates methotrexate-induced liver injury and suppresses hepatic stellate cells activation in rats: imperative role of Nrf2/NF-κB/NLRP3 signaling axis.

Mangifera indica (family Anacardiaceae), often acknowledged as mango and renowned for being a plant of diverse ethnopharmacological background since ancient times, harbors the polyphenolic bioactive constituent, mangiferin (MNG). MNG is a major phytochemical of Mangifera indica and other plants with a wide range of reported pharmacological activities, including antioxidant, anti-inflammatory, neuroprotective and hepatoprotective effects. MNG has also been utilized in traditional medicine; it is reportedly a major bioactive element in over 40 polyherbal products in traditional Chinese medicine (TCM), and two prominent anti-inflammatory, immunomodulatory and antiviral Cuban formulations. Despite the availability of evidence in support of MNG hepatoprotective properties, its hepatoprotective potential against MTX-induced liver injury and fibrosis has not been explored yet. To unravel the hepatoprotective potential of MNG against MTX-induced hepatic injury and fibrosis and elucidate the possible underlying molecular mechanisms. Male Sprague-Dawley rats were, randomly, distributed into five groups; two of which were administered MNG 50 mg/kg and MNG 100 mg/kg intraperitoneally (i.p.) for ten days, and a single i.p. injection of MTX 40 mg/kg on the seventh day to establish hepatotoxicity. Blood and liver tissue samples were retrieved from all study groups and analyzed for liver functions, histopathological alterations, and oxidative stress, inflammatory, and fibrotic biomarkers. MNG restored the MTX-induced degenerations in hepatic architecture and function. Moreover, it combated the MTX-elicited oxidative stress evidently by the significantly attenuated hepatic tissue levels of malondialdehyde, and the significantly elevated reduced glutathione and Nrf2 levels. MNG also halted inflammation depicted by the downregulation of the NF-κB/NLRP3 inflammasome axis. It further demonstrated anti-fibrogenic potential as evidenced by the significant reduction in fibrous tissue deposition and hepatic expression of α-SMA. The current study proved the hepatoprotective, and anti-fibrogenic effects of MNG against MTX-induced hepatotoxicity via the downregulation of NF-κB/NLRP3 inflammasome signaling axis, preceded by the amelioration of oxidative stress and Nrf2 signaling upregulation.

Antioxidant Effects of Moringa oleifera Against Abamectin-Induced Oxidative Stress in the Brain and Erythrocytes of Rats.

The current study was conducted to explore the phytochemical composition and in vitro antioxidant activity of Moringa oleifera leaves aqueous extract (MOLE), as well as its in vivo modulatory effects on abamectin (ABM)-induced oxidative stress in rat erythrocytes and brain tissue. Following extraction, the total phenolic, flavonoid, condensed tannin and ortho-diphenolic contents of MOLE were determined. High-performance liquid chromatography (HPLC) analysis allowed the identification and the quantification of 12 bioactive compounds: gallic acid, chlorogenic acid, caffeic acid, vanillic acid, quercetin, ferulic acid, ascorbic acid, alizarin, hesperidin, neohesperidin, resveratrol, and naringin. In vitro study: the assessment of the antioxidant activity of MOLE on the 2,2-diphenyl-1-picrylhydrazyl radical DPPH and the 2,2'-azino-bis(3-ethylbenzothiazoline-6-sulfonic acid) radical cation (ABTS), its ferric reducing power and its antioxidant effect on the β-carotene bleaching indicated that MOLE exhibited potent antioxidant activity, with an IC50 of 0.125mg/mL against DPPH radical, and an IC50 of 0.06mg/mL against ABTS radical. It also demonstrated notable ferric-reducing ability, with an EC50 of 1.4mg/mL and a strong inhibition of β-carotene bleaching with an IC50 of 1.36mg/mL. In vivo study: Twenty rats were equally divided into four groups. The first group served as a control and received distilled water by gavage. The second group (negative control) received ABM in drinking water at a dose of 1mg/kg body weight. The third group received MOLE at a dose of 200mg/kg of body weight by gavage. The fourth group received a combination of ABM and MOLE in the same manner and doses as described, for 3weeks. Body weight, brain relative and absolute weights, and nitric oxide levels were not affected by ABM. However, ABM significantly inhibited acetylcholinesterase (AChE) activity (p<0.001), decreased the activities of antioxidant enzymes, specifically superoxide dismutase (SOD) and glutathione S-transferase (GST) in cerebral tissue, and catalase (CAT) in erythrocytes (p<0.001). ABM also decreased reduced glutathione (GSH) levels in both the brain (p<0.001) and erythrocytes (p<0.05). In addition, malondialdehyde (MDA) levels significantly increased in the brains of ABM-intoxicated rats (p<0.01) compared to the control group. These results were accompanied by histopathological changes, notably the remarkable vacuolization of neuropil in brain tissue. Supplementation with MOLE in ABM-treated rats significantly ameliorated brain AChE (p<0.05) and GST activities, decreased MDA content, and improved GSH levels in both brain and erythrocyte homogenates (p<0.01). MOLE also restored the histopathological alterations observed in the ABM group. Computational modeling revealed that some of the tested molecules, including some present in the studied extract, bound human peroxiredoxin 5, CAT, and glutathione peroxidase with acceptable affinities, which, together with the established molecular interactions and tight embedding satisfactory support the in vivo results. Thus, it may be concluded that ABM impairs brain and erythrocyte function through oxidative damage, and these effects could be prevented by MOLE, likely due to its antioxidant activity.

Diethyl nitrosamine-induces neurobehavioral deficit, oxido-nitrosative stress in rats' brain: a neuroprotective role of diphenyl diselenide.

Diethylnitrosamine (DEN), a common dietary carcinogen, is associated with neurotoxicity in humans and animals. This study investigated the neuroprotective effects of diphenyl diselenide (DPDS) against DEN-induced neurotoxicity in male Albino Wistar rats (n = 40). Rats were randomly distributed into cohorts and treated as follows: vehicle control (corn oil 2mL/kg; gavage), DPDS-only (5mg/kg; gavage) and DEN-only (200mg/kg; single dose i.p.). Also, two other rat cohorts were pre-treated with DPDS (3 or 5mg/kg) for 15days (day: 0-15), subsequently administered with DEN (200mg/kg) and continuously treated with DPDS for another 7days, (days:15-21). Behavioural tests (OFT- using the open field test; NORT- novel object recognition test; FST- forced swimming test and Y-maze) were conducted from days 19-21, followed by biochemical analysis of the hippocampus and prefrontal cortex for oxidative stress, inflammation, neurotransmitter metabolic enzyme, and histopathology. DEN-treated rats exhibited decreased locomotor activity, spatial memory function and antioxidant activity, increased oxidative and nitration stress, anxiety, and depressive-like behaviour, causing histoarchitectural damage in prefrontal and hippocampal cortices. DPDS treatment (pre- and post-DEN exposure) significantly alleviated these neurotoxic, oxidative, and nitration effects, reversed DEN-induced histopathological alterations, and improved locomotive and cognitive functions. In conclusion, DPDS demonstrates potent neuroprotective effects against DEN-induced toxicity, likely through enhanced endogenous antioxidant capacity that mitigates oxido-nitrative damage. These findings suggest that the organo-selenium -DPDS- is a promising chemotherapeutic agent potent in alleviating DEN-mediated neurotoxicity and maintaining brain health.

Symbiotic bacteria associated with entomopathogenic nematodes showed molluscicidal activity against Biomphalaria glabrata, an intermediate host of Schistosoma mansoni

BackgroundBiomphalaria glabrata acts as the intermediate host of schistosomes that causes human schistosomiasis. Symbiotic bacteria, Xenorhabdus and Photorhabdus associated with Steinernema and Heterorhabditis, produce secondary metabolites with several biological activities. Controlling B. glabrata is a potential strategy to limit the transmission of schistosomiasis. The aims of this study were to identify Xenorhabdus and Photorhabdus bacteria based on recA sequencing and evaluate their molluscicidal activity against B. glabrata snail.ResultsA total of 31 bacterial isolates belonging to Xenorhabdus (n = 19) and Photorhabdus (n = 12) (X. ehlersii, X. stockiae, X. indica, X. griffinae, P. luminescens, P. akhurstii, and P. laumondii subsp. laumondii were molecularly identified based on recA sequencing. Five isolates of bacterial extracts showed potential molluscicide, with 100% snail mortality. P. laumondii subsp. laumondii (bALN19.5_TH) showed the highest effectiveness with lethal concentration (LC) values of 54.52 µg/mL and 89.58 µg/mL for LC50 and LC90, respectively. Histopathological changes of the snail were observed in the head–foot region, which showed ruptures of the epithelium covering the foot and deformation of the muscle fiber. A hemocyte of the treated snails was observed in the digestive tubules of the digestive glands. The hermaphrodite glands of treated snails showed a reduction in the number of spermatozoa, degeneration of oocytes, and deformation and destruction in the hermaphrodite gland. In addition, liquid chromatography–tandem mass spectrometry (LC–MS/MS) of three symbiotic bacteria contained compounds such as GameXPeptide, Xenofuranone, and Rhabdopeptide.ConclusionsFive bacterial extracts showed good activity against B. glabrata, especially P. laumondii subsp. laumondii and X. stockiae, which produced virulent secondary metabolites resulting in the death of the snails. They also caused histopathological alterations in the foot, digestive glands, and hermaphrodite glands of the snails. This study suggests that extracts from these bacteria show promise as molluscicides for the control of B. glabrata.Graphical abstract

Short-chain fatty acids as a novel intervention for high-fat diet-induced metabolic syndrome.

Metabolic syndrome (MetS) is driven by a complex interplay of genetic, lifestyle, and dietary factors, leading to weight gain, insulin resistance, dyslipidemia, and chronic inflammation. Gut microbiota dysbiosis has been recently recognized as a key contributor to MetS, leading to advancements in gut microbiome-based interventions to improve health outcomes. Considering the unique challenges associated with the use of pre/probiotics, short-chain fatty acids (SCFA), also known as postbiotics, have emerged as promising therapeutic agents due to their role in modulating host metabolism and physiology. Considering this, the aim of the current study was to explore the therapeutic potential of SCFA (butyrate, propionate, and acetate) supplementation against a high-fat diet (HFD)-induced experimental model of MetS in male Wistar rats. Alterations in body weight, lipid profile, histopathology, and adipose tissue accumulation were assessed to establish SCFA-mediated amelioration of experimental MetS. Further, the enzymatic (GPx, Catalase, GR, and GST) and non-enzymatic (LPO, total ROS, and Redox ratio were evaluated. The results indicated that SCFA supplementation could effectively mitigate key features of MetS. A significant reduction in body weight gain and fasting blood glucose levels, along with markedly lowered triglycerides, total cholesterol, and LDL levels, with partial restoration of HDL levels was observed following SCFA supplementation. SCFA administration also attenuated MetS-associated hepatic damage as studied by histopathological investigation and analysis of liver function marker enzyme activities. Such ameliorative effects of SCFA against HFD-induced MetS were owed to potential redox modulation studied using enzymatic and non-enzymatic oxidative stress markers. In conclusion, the study's outcomes show that SCFA supplementation could potentially be used against managing MetS. It underscores the therapeutic potential of SCFA by placing them as a novel gut microbiome-based dietary approach to improve metabolic health and reduce the risk of MetS-associated complications. However, more detailed mechanistic explorations are warranted in the future, leading to their beneficial role in MetS contributing to holistic health outcomes.

A rare perspective: fine-needle aspiration cytologic features of hyaline vascular type of Castleman disease: A case report.

Castleman disease, also known as Castleman syndrome, is a rare, nonmalignant lymphoproliferative disorder. The localized subtype of this disease is primarily the hyaline vascular type of Castleman disease (HVCD). Although this disease is a benign lesion, the histologic features are similar to those of some malignant lymphomas, so an accurate diagnosis of the disease is required. Lymph node hyperplasia lesions are usually diagnosed mainly by relying on biopsy histopathology, but the surgical process is time-consuming and expensive, and a part of patients usually refuse to undergo this examination method. Fine-needle aspiration cytology (FNAC) is a convenient, rapid, minimally invasive test for surface masses, and patients often receive cytopathology results in as little as a few minutes. Currently, there are few reports on the pathological features of FNAC in HVCD, so our cytopathological experience of using FNAC for rapid diagnosis of HVCD and other diseases that need to be differentiated are described in detail to give some meaningful references to the pathologists in recognizing HVCD from a rare cytological point of view. A late 50s female patient presented to the hospital with a single subcutaneous enlarged nodule in the right side of the neck, which had been present for >6 months. The nodule exhibited a relatively clear border, and the patient presented with no signs of pain, no skin damage, and no other notable symptoms, but was concerned about the benignity or malignancy of the enlarged nodule. To determine the exact diagnosis of the neck nodule, the patient first underwent FNAC, followed by surgical excision of the neck nodule for histopathologic examination. Since HVCD is a benign lesion and the superficial neck nodes were removed by minimally invasive surgery, the patient did not receive any other interventions. We successfully and accurately diagnosed the rare HVCD using FNAC. Histologically similar lesion features of HVCD were successfully observed in cytology. The cytologic pattern of HVCD is distinctly different from that of other benign lymphoid tissue proliferative lesions or metastatic carcinomas. This case shows important cytologic features for the diagnosis of HVCD using FNAC. The FNAC results showed abundant follicular dendritic cells and transparent blood vessels, and these cytologic features recapitulate the histopathologic alterations that were seen in HVCD. So by observing these cytologic features can help us to make an accurate diagnosis of HVCD using FNAC.

Rosmarinic acid protects against cyclophosphamide-induced hepatotoxicity via inhibition of oxidative stress, inflammation, and apoptosis and upregulation of Nrf2 in mice.

Cyclophosphamide (CP) is widely used in chemotherapy to treat various types of cancer. However, it is toxic to the liver and other organs. Rosmarinic acid (RA) possesses anti-inflammatory, antioxidant, and cytoprotective properties. This study investigated the protective effects of RA against CP-induced liver injury in mice. Mice were treated with RA (25, 50, and 100mg/kg) for 15days and followed by a single injection of CP on day 16th. CP injection resulted in an elevation in serum AST, ALT, and ALP, along with multiple histopathological alterations in the liver. CP also induced increased levels of MDA and NO, associated with declined GSH, SOD and CAT. RA pretreatment prevented liver injury, alleviated the enhanced levels of MDA and NO, and restored antioxidants defenses, hence avoiding the oxidative injury in the liver. Moreover, RA pretreatment attenuated NF-κB p65 and proinflammatory cytokines levels. Liver of CP-injected mice also showed a decrease in Bcl2, accompanied with elevated BAX and caspase-3 expression, an effect that RA pretreatment alleviated. In addition, pretreatment of CP-administrated mice with RA restored the Nrf2 expression in the liver. Taken together, this study suggests a potential application value of RA in preventing CP hepatotoxicity and sheds light on the possible mechanism.

Effects of the Interaction of Salinity and Rare Earth Elements on the Health of Mytilus galloprovincialis: The Case of Praseodymium and Europium.

The growing use of products containing rare earth elements (REEs) may lead to higher environmental emissions of these elements, which can potentially enter aquatic systems. Praseodymium (Pr) and europium (Eu) are widely used REEs with various applications. However, their ecotoxicological impacts remain largely unexplored, with poorly understood risks to wildlife. Moreover, organisms also face environmental stressors like salinity fluctuations, and the nature of the interaction between salinity variations and contaminants is not yet clear. Therefore, this study aimed to evaluate the influence of salinity shifts on the impacts of Pr and Eu on adult mussels and the sperm of the species Mytilus galloprovincialis after 28 days and 30 min of exposure, respectively. To do so, biochemical and histopathological alterations were evaluated in adults, while biochemical and physiological changes were analysed in sperm. Additionally, the Integrated Biological Index (IBR) was calculated to understand the overall impact of each treatment. The results showed that adult mussels were most affected when exposed to the combination of high salinity and each element, which altered the behaviour of defence mechanisms causing redox imbalance and cellular damage. On the other hand, sperm demonstrated sensitivity to specific REE-salinity combinations, particularly Pr at lower salinity and Eu at higher salinity. These specific treatments elicited changes in sperm motility and velocity: Pr 20 led to a higher production of O2- and a decrease in velocity, while Eu 40 resulted in reduced motility and an increase in irregular movement. At both lower and higher salinity levels, exposure to Eu caused similar sensitivities in adults and sperm, reflected by comparable IBR scores. In contrast, Pr exposure induced greater alterations in sperm than in adult mussels at lower salinity, whereas the reverse was observed at higher salinity. These findings suggest that reproductive success and population dynamics could be modulated by interactions between salinity levels and REE pollution, highlighting the need for further investigation into how REEs and environmental factors interact. This study offers valuable insights to inform policymakers about the potential risks of REE contamination, emphasising the importance of implementing environmental regulations and developing strategies to mitigate the impact of these pollutants.