Increase In MDA Levels Research Articles

Effects of gestational diabetes mellitus and diabetes mellitus on lipid profile, antioxidants, hormones and electrolytes status in a population of Nigerian women

AimGestational diabetes mellitus (GDM) cases are rising globally. This research examined the effects of GDM and diabetes mellitus whose hallmark is hyperglycemia on hormones, lipid profiles, electrolytes and antioxidants in freshly diagnosed women attending teaching hospitals in Ekiti State, Nigeria.MethodsThe cross-sectional design followed convenience sampling in four groups (n = 50): gestational diabetes women (GDM), normal pregnant women (NP), diabetes nonpregnant women (DM) and nondiabetes nonpregnant women (ND-NP). Blood samples were collected from fasting subjects through antecubital fossa. BMI, FPG, TC, TG, LDL-C, HDL-C, sodium, potassium and bicarbonate ions, MDA and antioxidants were investigated using standard procedures and spectrophotometer. Results were analysed using one-way ANOVA and p < 0.05 was used as significant difference.ResultsThere was significant (p < 0.05) increase in FPG of GDM and DM (> 5.56 mmol/l) subjects compared to NP and ND-NP subjects. TC, TG, HDL-C and LDL-C were elevated in GDM and DM groups compared to NP and ND-NP groups. Sodium ion concentration was significantly (p˂0.05) elevated in ND-NP group relative to GDM and DM groups. There was significant (p < 0.05) increase in MDA levels in DM and NP groups compared to ND-NP. Superoxide dismutase activity was significantly (p < 0.05) greater in ND-NP than in DM and NP. Progesterone level was greater in GDM group than in other groups. The FSH concentration was lower in the GDM and NP groups than in the DM and ND-NP groups, and prolactin concentration was greater in the GDM group than in the NP.ConclusionThis study suggested that GDM and DM could result in hormonal and electrolyte imbalances, elevated lipid profiles, and reduced antioxidant levels.

The ultrastructural changes in the adult rat ovary after administration of copper oxide nanoparticles and the possible ameliorative influence of selenium

ABSTRACT There is an important concern about the potential health and environmental risks that may develop due to exposure to copper oxide nanoparticles (CuO-NPs). Selenium is an essential trace element. It supports the expression of a variety of selenoproteins. The present study was designed to study the ultrastructural and biochemical changes in the adult rat ovary after oral administration of CuO-NPs and to assess the possible ameliorative influence of Selenium. Sixty adult female albino rats were divided in two major groups: Group I and Group II. Group I was further subdivided into three groups: Group IA (control), Group IB: received a single high dose of 2000 mg/kg CuO-NPs, Group IC: received selenium (0.5 mg/kg), five days before giving a single high dose of CuO-NPs (2000 mg/kg). Thereafter, given selenium for 14 days. Group II was subdivided into three groups: Group IIA (control), Group IIB: received a small dose of 300 mg/kg of CuO-NPs for 28 days, Group IIC: received selenium (0.5 mg/kg), five days before starting concomitant administration of CuO-NPs (300 mg/kg) and Selenium (0.5 mg/kg) for 28 days. Damage of the ovarian ultrastructural features, increased MDA levels, and decreased serum estrogen and progesterone hormones levels were detected in group IB and group IIB. Group IC and group IIC showed improvement of ovarian ultrastructural, decreased MDA levels, and increased serum estrogen and progesterone hormones levels as compared to group IB and group IIB indicating that Selenium could decrease the damage induced by CuO-NPs in the adult rat ovaries.

The effect of resveratrol on lead-induced oxidative damage and apoptosis in HT-22 cells.

The purpose of this work was to investigate whether resveratrol affects lead-induced oxidative damage in HT-22cells, characterizing mechanisms and strategies for preventing and treating lead-induced neurotoxicity. Various lead and resveratrol concentrations were applied to HT-22cells over different time periods. First, we established the lead treatment (12.5, 50 and 200μmol/L) and resveratrol (40μmol/L) intervention model for the study. MTT was used to analyze HT-22cell survival rate. The rates of cell death, mitochondrial membrane potential, lipid peroxidation, and reactive oxygen species (ROS) generation were all measured by flow cytometry. Cellular oxidant (MDA) and antioxidant (SOD, GSH-Px) levels were measured with test kits. Western blotting was used to assess the expression of proteins related to autophagy and apoptosis. Lead reduced HT-22cell viability in a concentration/time-dependent manner. In addition, lead (200μmol/L) decreased the protein expression of BCL2, while increasing PARP and BAX expression and apoptotic rate. Moreover, the lead-exposed group had significantly higher levels of ROS, lipid-ROS, and MDA than the control group. This was accompanied by increased MDA levels and decreased SOD, GSH-Px, and MMP levels in the lead-exposed cells. Furthermore, lead lowered SIRT1 protein expression, while increasing the levels of autophagy-related proteins, including P62, ATG5, Beclin-1 and LC3 Ⅱ/Ⅰ. Resveratrol (40μmol/L), an agonist of SIRT1, restored the effects of lead (200μmol/L) to levelsindistinguishable from controls. Resveratrol inhibited mitochondrial damage and restored the lead-induced block of autophagic flux and oxidative stress by activating SIRT1, thereby alleviating lead-induced damage in HT-22cells.

Maternal exposure to nicotine causes oxidative stress and inflammatory changes in the ovaries of rats' adult offspring.

Nicotine is one of the most toxic substances found in cigarettes, but also found in chewing tobacco gum, patches and vaping products (electronic cigarettes). In addition to being a highly addictive chemical, it is capable of reducing fertility in men and women. In the ovaries, it can induce morphological changes and impair the formation of follicles, being a possible cause of changes in the reproductive cycle and anticipation of menopause in women whose mothers smoked during pregnancy. By increasing the generation of free radicals, nicotine can induce oxidation in biological samples and change the expression of inflammatory cytokines. It damages the immune system and many other cells of newborns exposed prenatally. Despite its teratogenic potential, many women continue to use this drug during pregnancy and lactation. Thus, this work aims to analyze the effects of maternal exposure to nicotine on the ovaries of adult rats. To this end, 10 rats received nicotine throughout pregnancy and lactation. Their offspring were euthanized around 90 days-old, in the metestrus phase, for ovary collection and analysis of oxidative stress and inflammation. The results showed that exposure to nicotine increased MDA level, but did not cause damage to the DNA of ovarian cells (8-OHdG). It also increased IL-1β and anti-inflammatory protein AnxA1 and receptor Fpr1, and reduced the mast cell population in ovaries. We concluded that maternal exposure to nicotine is capable of inducing oxidative stress and leading to inflammatory changes in the ovaries of adult offspring exposed during the intrauterine and breastfeeding phases.

520 nm and 660 nm light-emitting diodes modulates pancreatic development and beta cell functions in zebrafish embryos.

Green and Red LEDs increase insulin production, but their comparative effects on pancreatic and beta cell development are unclear. Zebrafish embryos were divided into three groups: Control (n = 60), Green (G) (n = 60), and Red (R) (n = 60), then irradiated for three days (14 hours/day) with 0.5 W/cm2 G (λpeak = 520 nm, 180 mA) and R (λpeak = 660 nm, 210 mA). At the end of 72 h, pancreatic and beta cells, circadian rhythm, and oxidative stress gene were analyzed using RT-PCR. Malondialdehyde, nitric oxide, superoxide dismutase, and glutathione levels were also evaluated. In the Red group, pancreatic area increased by ~97.13% compared to the Control group and by approximately ~62.16% compared to the G group (both p < 0.0001), and no significant difference in beta cell area (p = 0.964). G group insulin expression increased 2.31-fold compared to R group (p < 0.0001). Red LED treatment increased MDA levels (p < 0.001), oxidative stress (fth1b, nqo1) (p < 0.0001), and per1b during the photophase (p < 0.0001) compared to G group. R LED treatment increases oxidative stress and disrupts circadian rhythm, leading to reduced insulin secretion. The positive effects of G LED treatment have potential for metabolic syndrome, diabetes, and pancreatic diseases.

Neuroprotective Effects of Thymol and p-Cymene in Immobilized Male rats through Alterations in Molecular, Biochemical, Histological, and Behavioral Parameters.

The research was conducted to examine the neuroprotective effect of thymol and its precursor p-cymene on chronic immobility stress in adult male Wistar rats. The rats were subjected to 2.5h of stress every day for 14 consecutive days by placing them inside a restrainer. Thymol (10mg/kg) and p-cymene (50mg/kg) were given to the rats during the same period. The results showed that thymol and p-cymene prevented the increase of MDA level, decline of GSH level, and decrease of SOD and GPx activity in the hippocampus of rats exposed to stress. These monoterpenes also prevented the increase in the expression of Tnfa, Il1b, Tlr4, and Nfkb, and the decrease in the expression of Nrf2, Ho1, and Bdnf. In addition, thymol and p-cymene inhibited the increase in the expression and activity of acetylcholinesterase in the hippocampus of animals exposed to immobility and enhanced the expression of A7nachr. They also reduced neuronal death in the CA1 region of stressed animals and improved their performance in the Morris water maze and elevated plus maze tests. Based on these findings, thymol and p-cymene may be effective in preventing neurodegenerative diseases as they reduce oxidative stress and neuroinflammation, strengthen ACh signaling, and stimulate Bdnf expression.

TLR2/TLR5 Signaling and Gut Microbiota Mediate Soybean-Meal-Induced Enteritis and Declined Growth and Antioxidant Capabilities in Large Yellow Croaker (Larimichthys crocea)

Soybean meal, renowned for its high yield, cost efficiency, and protein richness, serves as a pivotal plant-based alternative to fish meal. However, high soybean meal inclusion in Larimichthys crocea diets is linked to enteritis and oxidative damage, with unknown mechanisms. Our study aims to elucidate the molecular basis of soybean-meal-induced enteritis and its impact on intestinal microbiota in L. crocea. To this end, four isonitrogenous and isolipidic diets with varying soybean meal levels (0% FM, 15% SBM15, 30% SBM30, and 45% SBM45) were administered to L. crocea for 8 weeks. The results indicated that the SBM30 and SBM45 treatments significantly hindered fish growth, digestive efficiency, and protein utilization. Furthermore, high soybean meal levels (SBM30 and SBM45) activated intestinal Toll-like receptors (TLR2A, TLR2B, TLR5, and TLR22), stimulating C-Rel and mTOR protein expression and elevating ERK phosphorylation. This led to increased pro-inflammatory cytokine production (IL-1β, IL-6, and TNF-α) and decreased anti-inflammatory cytokine expression (IL-4/13A, IL-4/13B, and TGF-β), suggesting a potential signaling pathway for soybean-meal-induced enteritis. Furthermore, enteritis induced by high soybean meal levels led to oxidative damage, evident from increased MDA levels and decreased antioxidant enzyme activities (SOD and CAT). The SBM30 and SBM45 treatments increased Firmicutes and Bacteroidetes abundance in fish gut microbiota, while Proteobacteria abundance decreased. This microbiota shift may enhance soybean meal nutrient utilization, yet high soybean meal concentrations still impair growth. A soybean-meal-rich diet promotes harmful bacteria like Rhodococcus and depletes probiotics like Ralstonia, increasing disease risks. L. crocea has limited tolerance for soybean meal, necessitating advanced processing to mitigate anti-nutritional factors. Ultimately, exploring alternative protein sources beyond soybean meal for fish meal replacement is optimal for L. crocea.

Ameliorative effects of pyrroloquinoline quinone on oxidized fish oil-induced growth retardation, immune suppression, and oxidative stress in yellow catfish Tachysurus fulvidraco

Fish oil is the primary oil source in aquafeeds, but is susceptible to oxidation during production and storage, thereby leading to oxidative stress in fish. Pyrroloquinoline quinone (PQQ) is a novel redox cofactor that possesses numerous pharmacological properties. Hence, the aim of this study was to evaluate whether dietary PQQ supplementation could alleviate stress response of yellow catfish (Tachysurus fulvidraco) caused by oxidized fish oil. Fish were fed four experimental diets containing fresh and oxidized fish oil either with or without PQQ (0 or 5 mg kg−1) supplementation for 8 weeks. Results revealed that dietary oxidized fish oil significantly decreased growth performance of fish, fat content in whole-body, and the immunological parameters. Also, it significantly elevated aspartate aminotransferase and alanine aminotransferase activities, as well as the levels of total cholesterol, triglyceride, and glucose in serum. Meanwhile, oxidized fish oil decreased antioxidant enzyme activities (superoxide dismutase and glutathione peroxidase) and total antioxidant capacity but increased MDA level in serum. However, the addition of PQQ in the oxidized fish oil diet could overcome the negative impacts of oxidized fish oil on yellow catfish and normalise the detected parameters nearly to the control values. Taken together, long-term feeding of oxidized fish oil diet destroyed liver, disordered lipid metabolism, diminished nonspecific immunity as well as caused oxidative stress, and eventually resulted in growth retardation of yellow catfish, whereas dietary PQQ supplementation had a significant ameliorative role in adverse effects induced by dietary oxidized fish oil, and therefore, may be recommended for use in aquaculture to prevent oxidized lipid.

Assessment of reproductive, genotoxic, and cytotoxic effects of leachate-contaminated water in male mice

Leachate-contaminated water (LCS) poses significant health risks due to its heavy metal content and altered physicochemical properties. This study examined the physicochemical parameters and heavy metal levels in LCS and assessed its reproductive toxicity, genotoxicity, and cytotoxic effects in exposed mice. Groups of mice (n = 5) were orally administered 100 μL of 30 % and 70 % LCS (v/v) twice daily for 35 days. Drinking water served as a negative control, and cyclophosphamide (Cyp) (20 mg/kg bw) as a positive control. On day 36, the mice were weighed, sacrificed, and their testicular weight, sperm count, sperm morphology, viability, acrosome integrity, and serum testosterone were examined. Oxidative stress in the testes, histopathological changes, and serum markers for liver and kidney function (SGOT, SGPT, and creatinine) were also assessed. Genotoxic effects were evaluated using a micronuclei (MN) assay. Analysis of the leachate showed altered physicochemical parameters and elevated heavy metal levels. Exposure to LCS led to a significant decrease in relative testis weight, sperm count, normal sperm morphology, viability, acrosome integrity, and serum testosterone levels. It also caused a notable increase in MDA levels and a decrease in catalase (CAT), superoxide dismutase (SOD), and glutathione (GSH) levels, along with histological changes in the testes of LCS-treated mice compared to controls. Additionally, there was a significant rise in MN formation in RBCs and elevated levels of liver enzymes and creatinine, indicating liver and renal toxicity. Histological alterations in the liver and kidneys were also observed in LCS-exposed mice. These findings suggest that LCS induces reproductive toxicity, genotoxicity, and cytotoxicity in male subjects.

Repurposing flubendazole for glioblastoma ferroptosis by affecting xCT and TFRC proteins.

New uses of old drugs hold great promise for clinical translation. Flubendazole, an FDA-approved antiparasitic drug, has been shown to target p53 and promote apoptosis in glioblastoma (GBM) cells. However, its damaging mechanism in GBM remains elusive. Herein, we explored the ferroptosis-inducing ability of flubendazole on GBM cells. After treating glioma cell lines U251 and LN229 with the flubendazole (DMSO <1‰), cell viability was inhibited in a concentration-dependent manner (IC50 for LN229 = 0.5331 μM, IC50 for U251 = 0.6809 μM), attributed to the induction of ferroptosis, as evidenced by increased MDA levels, accumulation of ROS and lipid peroxides, change in mitochondrial membrane potential and structure. Protein analysis related to ferroptosis showed upregulation of TFRC, DMT1 and p53, alongside downregulation of xCT, FHC and GPX4 (p < 0.05). All-atom docking studies demonstrated that flubendazole bound closely with xCT, and TFRC, validating its role in inducing glioma ferroptosis via modulation of these proteins. Notably, flubendazole could damage the glioblastoma stem cells (GSC) that are typically resistant to other therapies, thereby possessing advantages in stopping glioma recurrence. This study delved into the mechanisms of flubendazole-induced ferroptosis in glioma, broadening its application and providing new ideas for new uses of other old drugs.

The Potential Health Risks of Catha edulis Forsk (Khat) Consumption on Some Vital Organs

Abstract Introduction/Objective Introduction: Catha edulis Forsk (Khat) leaves are widely chewed by adults in the Arabian Peninsula and the Horn of Africa for their mild stimulating properties. Objectives To investigate the impact of an aqueous extract of Catha edulis Forsk leaves on the proper functioning of vital organs. Methods/Case Report Methods: Materials and methods: Twenty-five female albino rats were divided into two groups: a control group and a treated group which received a daily gavage of 1 ml of aqueous Khat extract with a concentration of 700 mg/kg body weight for four weeks. The effects of this treatment on selected organs, including the brain, hippocampus, heart, and ovaries, were assessed using various measurements and analyses. Results (if a Case Study enter NA) Results: Results: The antioxidant evaluation showed a significant increase in MDA levels in the khat group and a significant decrease in GSH, SOD, and CAT levels compared to the control group. There was a significant decrease in IL-4 and a significant increase in TNF-α and TGF-β1 compared to the control group. In contrast, the cardiac enzymes; Troponin, CK, CPK, and GOT showed a significant increase compared to the control group. The results of the hormonal assay indicated a significant increase in LH, FSH, and testosterone levels, along with a significant decrease in estrogen in the khat group compared to the control group. Furthermore, the histological investigations revealed significant changes in tissue architecture in the studied organs. In the heart, the treated group exhibited an intact, thick pericardium, along with markedly apoptotic cardiac muscle fibers and others with pyknotic nuclei and mildly congested blood vessels and capillaries. The examination of brain tissues in the treated group showed thick meninges with mild inflammatory infiltrate, marked astrogliosis with degenerated neurons in the cerebral cortex, inflammatory infiltrate with abscess formation and mildly congested blood vessels and eosinophilic plaque-like area in the deep cortex, and scattered degenerated neurons and some neurons with nuclear vacuoles and average glial cells in the white matter. In the ovaries, sections showed primary, secondary, and antral follicles, scattered cystically dilated follicles with atrophied lining, and multiple corpora lutea in the edematous stroma with scattered apoptotic stromal cells. Conclusion Based on these findings, long-term use of khat as a chewing material may harm vital organs.

Curcumin promotes ferroptosis in hepatocellular carcinoma via upregulation of ACSL4

BackgroundFerroptosis, a novel iron-ion-dependent metabolic cell death mode with lipid peroxides as the main driving substrate, plays an irreplaceable role in the development and preventive treatment of hepatocellular carcinoma. Curcumin has potent pharmacological anti-tumor effects.Aim of the studyWe aimed to evaluate the ex vivo and in vivo cancer inhibitory activity of curcumin and its specific mechanism of action.Materials and MethodsWe used the hepatocellular carcinoma cell lines HepG2 and SMMC7721 to assess the direct inhibition of hepatocellular carcinoma proliferation by curcumin in vitro and a tumor xenograft model to evaluate the in vivo cancer inhibitory effect of curcumin.ResultsIn this study, we found that ferroptosis’s inhibitors specifically reversed the curcumin-induced cell death pattern in HCC. After curcumin intervention, there was a substantial increase in MDA levels and iron ion levels, and a decrease in intracellular GSH levels. Meanwhile, the expression of GPX4 and SLC7A11 was significantly reduced at the protein levels, while ACSL4 and PTGS2 expression was significantly increased.ConclusionsThis study showed that curcumin significantly decreased the proliferation of HCC cells and significantly increased the sensitivity of ferroptosis. These results suggest that ACSL4 is a viable target for curcumin-induced ferroptosis in treating HCC.

Neuroinflammation and oxidative redox imbalance drive memory dysfunction in adolescent rats prenatally exposed to Datura Stramonium

Although there have been reports indicating that Datura Stramonium (D. stramonium) may induce anticholinergic and neuropsychiatry effects, the compound is still being used for recreational and medicinal purposes while ingestion during pregnancy has been documented. Intriguingly, minimal studies have investigated the potential neurotoxic impact of D. stramonium exposure at various stages of gestation, including its potential implication on neurophysiological well-being later in life. The present study, therefore, examined spontaneous working memory and the expression of specific neurochemicals modulating crucial neural processes in adolescent rats exposed to high and low D. stramonium doses during different stages of gestation. Pregnant rats were orally infused with 150- or 500- mg/kg/day of D. stramonium either during mid- (second week; days 8–14) or late- (third week; days 15–21) gestation, while control rats received PBS at dosing periods. Behavioral characterization of offspring between postnatal days (PD) 40 and 41 in the Y-maze revealed that D. stramonium perturbed spatial working memory in rats, although locomotor activity was generally unaltered. In addition to SOD and nitric oxide downregulation, induction of oxidative stress in the hippocampus and prefrontal cortex (PFC) of young adult rats prenatally exposed to D. stramonium was corroborated by depletion of key antioxidant regulatory elements glutathione peroxidase, glutathione reductase and catalase, which was accompanied by lipid peroxidation shown by increased MDA levels. Whereas increased expression of acetylcholinesterase and LDH was seen in adolescent rats prenatally infused D. stramonium, acetylcholine levels were downregulated in both hippocampal and PFC lysates, suggesting cholinergic and metabolic dysfunctions. Immunohistochemical labelling of GFAP and IBA-1 revealed increased expression of reactive astrocytes and microglia respectively, while the accompanying TNFα upregulation in both the hippocampus (dentate gyrus) and PFC causally linked intrauterine D. stramonium exposure with neuroinflammatory responses postnatally. Overall, our data correlated postnatal spatial working memory dysfunction evoked by D. stramonium exposure during critical stages of embryonic development to oxidative redox impairment, cholinergic disruption and neuroinflammatory perturbations in rats.

Biochemical responses of crayfish exposed to imidacloprid: assessment of oxidative stress, osmoregulatory response and neurotoxicity

ABSTRACT Among the nicotinoid insecticides, imidacloprid (IMI) may affect non-target invertebrates like aquatic crustaceans by entering the aquatic environment through rainfall. Nevertheless, there are not sufficient studies on the toxicity mechanism of IMI in crayfish. Here, we investigated the effects of IMI on oxidative stress, osmoregulatory, and neurotoxicity biomarkers. The 96-hour lethal concentration value (96 h-LC50) of IMI was determined to be 0.932 mg AI L−1. Four concentrations of IMI (0.932, 0.466, 0.233 and 0.117 mg AI L−1) were applied to crayfish for 96 h. Na+/K+-ATPase, Mg2+-ATPase, Ca2+-ATPase, and total ATPase activities had almost significantly concentration-related inhibition in both gill and muscle tissues (p < 0.05). Compare with control in hepatopancreas, the activities of GST, SOD and GPx were increased, while the activities of AChE, CES and GR were decreased (p < 0.05). As non-enzymatic parameters, a statistically significant (p < 0.05) increase in MDA levels and a decrease in GSH levels were observed in the hepatopancreas compared to the control group, which was not related to the concentration. In conclusion, it can be said that the study's biomarkers are highly helpful and that commercially consumed crayfish are a significant non-target organism in the assessment of IMI toxicity.

Neuroprotective Effects of Bryophyllum pinnatum against Ketamine-Induced Neurotoxicity in Wistar Rats: Neurochemical, Oxidative Stress, and Histological Investigation

Background: This study evaluated the neuroprotective effects of Bryophyllum pinnatum (B. pinnatum) in ketamine-induced neurotoxicity in Wistar rats, focusing on neurochemical and oxidative stress markers, as well as histological changes in the hippocampus and cerebral cortex. Methods: Sixty male Wistar rats were divided into six groups. Group 1 received normal saline (2ml), Group 2 was administered ketamine (20mg/kg), and Group 3 received risperidone (0.5mg/kg). Groups 4, 5, and 6 were treated with B. pinnatum at 50mg/kg, 100mg/kg, and 200mg/kg, respectively for a duration of 21 days after induction of toxicity. Neurochemical markers (dopamine, glutamate, GABA, serotonin, noradrenaline, acetylcholine), oxidative stress markers (GSH, MDA, SOD, CAT, GPx), and histological analysis of brain tissues were evaluated after treatment periods of one, two, and three weeks. Results: Ketamine administration significantly reduced dopamine, GABA, serotonin, and noradrenaline levels while increasing acetylcholine and glutamate levels (p&lt;0.05). B. pinnatum treatment reversed these effects in a dose-dependent manner, particularly at high doses. Oxidative markers showed reduced GSH and increased MDA levels with ketamine, which B. pinnatum mitigated significantly (p&lt;0.05). Histologically, ketamine caused neuronal degeneration and microstructural distortion in the hippocampus and cerebral cortex, which were markedly reduced by B. pinnatum, especially at 200mg/kg, showing well-preserved neuronal structures. Conclusion: B. pinnatum demonstrates significant neuroprotective effects against ketamine-induced neurotoxicity by modulating neurochemical and oxidative markers and preserving histological integrity in brain tissues, suggesting its potential therapeutic application in neurotoxic conditions.

Coconut oil affects aging-related changes in Mongolian gerbil liver morphophysiology

Aging causes changes in liver morphophysiology, altering hepatocyte morphology and organ function. Due to its antioxidant and anti-inflammatory properties, coconut oil has been used as a therapeutic agent in diets, in an attempt to attenuate alterations in the liver naturally caused by aging. Herein, we evaluated the effects of coconut oil consumption during aging on Mongolian gerbil liver morphophysiology. The animals were divided into three experimental groups: the gerbils in the Adult Control Group (AC) were euthanized at 3 months of age, the gerbils in the Old Control Group (OC) at 15 months of age, and the gerbils in the Coconut Oil Group (CO) received 0.1 ml/day of coconut oil for 12 months and were euthanized at 15 months of age. Prolonged consumption of coconut oil during aging prevented the animals and the liver from gaining mass. However, the other results showed that coconut oil intensified the morphophysiological alterations of aging, promoting an increase in the hepatocyte cytoplasm and nuclei. In addition, an increase in blood vessels, reticular fibers, lipid droplets, and lipofuscin granules were observed in the CO group. Finally, the results also demonstrated that coconut oil promotes an increase in lipid peroxidation, indicated by an increase in MDA levels. We therefore conclude that coconut oil has the potential to intensify the morphophysiological alterations that occur in the liver during aging.

Tannin-Rich Fraction of Cyperus esculentus Protects against Lead-Induced Testicular Toxicity in Male Wistar Rats through ITS Antioxidant Properpty

Aims: Lead as a common environmental toxic metal, causes many histological, physiological and biomedical abnormalities in human and animals. This study evaluated the antioxidant potential of tannins on serum level of testosterone, LH and FSH and histology of the testes of male Wistar rats. Materials and Methods: Twenty-five adult male Wistar rats were divided into five (5) groups, (n=5). Group NS was administered normal saline only, Group PBO was administered with 30mg/kg body weight (BW) of lead, group LDTPB was administered with 50 mg/kg BW of tannins and 30mg/kg BW of lead, group MDTPB was administered with 100mg/kg BW of tannins and 30mg/kg BW of lead, group HDTPB was administered 150mg/kg BW of tannins and 30mg/kg BW of lead orally for 28 days. The animals were sacrificed and testes were harvested on day 29 of the experiment and histological and histochemistry studies done using the H&amp;E and VVG staining respectively. Sperm parameters (motility, concentration), sex hormones (Testosterone, LH, FSH) and antioxidant activities were also determined. Results: There was Leydig cell proliferation and an increase series of spermatogenesis of the testes in the rats of groups administered with lead and tannins different doses (LDTPB, MDTPB and HDTPB) when compared with rats administered with lead only. Rats in groups LDTPB, MDTPB and HDTPB had a significant increase in levels of serum testosterone (p&lt;0.05) when compared with positive control group (2). There was increase in levels of FSH in MDTPB and HDTPB groups when compared with positive control (2). Increased MDA levels were observed in the rats given lead only, PBO when compared to NS group. The rats given lead and tannins significant growth of seminiferous epithelium, improved sperm quality, and had decreased MDA levels. Conclusion: This study demonstrated the protective role of tannins fraction of Cyperus esculentus on lead-induced testicular toxicity in male Wistar rats.

Insights into the response mechanisms of Tetradesmus obliquus to aged polylactic acid and tetracycline exposure via transcriptome analysis and physiological evaluations

Microplastics (MPs) and antibiotics, identified as emerging pollutants, are extensively prevalent in aquatic environments and display prolonged durability. Unlike conventional plastics, biodegradable plastics are more susceptible to decomposition in the environment, resulting in the generation of microplastics and posing potential risks to the aquatic ecosystems. In this study, we assessed growth inhibition, chlorophyll a content, malondialdehyde content (MDA), and antioxidant enzyme activities. These measurements were integrated with transcriptome analysis to explore the response mechanisms of virgin and aged polylactic acid (vPLA and aPLA) and tetracycline (TC) following 14-day exposure to Tetradesmus obliquus, either individually or in combination. The findings indicated that exposure to vPLA did not significantly impact the growth of T. obliquus. Conversely, aPLA demonstrated growth-promoting effects on T. obliquus, particularly in the latter incubation stages. Moreover, a 14-day exposure significantly increased the chlorophyll a content and the activities of superoxide dismutase (SOD), catalase glutathione (CAT) and glutathione S-transferase (GST) within the algal cells. Apart from 1 mg L−1, the TC concentrations of 2.5, 5.0, and 10 mg L−1 exhibited significant toxic effects on T. obliquus, including growth inhibition, decreased chlorophyll a content, elevated activities of SOD, CAT, and GST, and increased MDA levels. Exposure to a combination of 300 mg L−1 aPLA and 5.0 mg L−1 TC, compared to solely 5 mg L−1 TC, demonstrated a notable reduction in TC toxicity to T. obliquus in the presence of aPLA. This was indicated by elevated algal cell density and chlorophyll a content, as well as a decrease in MDA content. Transcriptome analysis indicated an enrichment of differentially expressed genes (DEGs) in pathways linked to porphyrin metabolism, photosynthesis, carbon fixation, and metabolism within the aPLA + TC combined exposure. The study aid in expanding our knowledge of the potential ecological risks posed by biodegradable plastics and accompanying pollutants in aquatic environments.

Aged fragmented-polypropylene microplastics induced ageing statues-dependent bioenergetic imbalance and reductive stress: In vivo and liver organoids-based in vitro study

Ageing is a nature process of microplastics that occurrs daily, and human beings are inevitably exposed to aged microplastics. However, a systematic understanding of ageing status and its toxic effect is currently still lacking. In this study, plastic cup lids-originated polypropylene (PP) microplastics were UV-photoaged until the carbonyl index (CI), a canonical indicator for plastic ageing, achieved 0.08, 0.17, 0.22 and 0.28. The adverse hepatic effect of these aged PPs (aPPs) was evaluated in Balb/c mice (75 ng/mL water, about 200 particles/day) and human-originated liver organoids (LOs, 50 particles/mL, ranged from 5.94 to 13.15 ng/mL) at low-dose equivalent to human exposure level. Low-dose of aged PP could induce hepatic reductive stress both in vitro and in vivo, by elevating the NADH/NAD+ratio in a CI-dependent manner, together with hepatoxicity (indicated by increased AST secretion and cytotoxicity), and disrupted the genes encoding the nutrients transporters and NADH subunits accompanied by the restricted ATP supply, declined mitochondrial membrane potential and mitochondrial complexI/IV activities, without significant increase in MDA levels in the liver. These changes in the liver disrupted systematic metabolism, representing a circulatory panel of increases in the lactate, triglyceride, Fgf21 levels, and decreases in the pyruvate level, linked the reductive stress to the declined body weight gain but elevated hepatic NADH contents following aPPs exposure. Additionally, assessing by the LOs, it was found that digestion drastically accelerated the ageing of aPPs and worsen the energy supply upon mitochondria, representing a “scattergun effect” induced by the formation of micro- and nano-plastics mixture toward NADH/NAD+imbalance.

Indole-3-acetic acid exposure leads to cardiovascular inflammation and fibrosis in chronic kidney disease rat model

Indole-3-acetic acid (IAA), a protein-bound uremic toxin, has been linked to cardiovascular morbidity and mortality in chronic kidney disease (CKD) patients. This study explores the influence of IAA (125 mg/kg) on cardiovascular changes in adenine sulfate-induced CKD rats. HPLC analysis revealed that IAA-exposed CKD rats had lower excretion and increased circulation of IAA compared to both CKD and IAA control groups. Moreover, echocardiography indicated that CKD rats exposed to IAA exhibited heart enlargement, thickening of the myocardium, and cardiac hypertrophy in contrast to CKD or IAA control group. Biochemical analyses supported the finding that IAA-induced CKD rats had elevated serum levels of c-Tn-I, CK-MB, and LDH; there was also evidence of oxidative stress in cardiac tissues, with a significant decrease in SOD and CAT levels, as well as an increase in MDA levels. The gene expression analysis found significant increases in ANP, BNP, β-MHC, TNF-α, IL-1β, and NF-κB levels in IAA-exposed CKD groups in contrast to the CKD or IAA control group. In addition, higher cardiac fibrosis markers, including Col-I and Col-III. The findings of this study indicate that IAA could trigger cardiovascular inflammation and fibrosis in CKD conditions.