Reduced Superoxide Dismutase Research Articles

Pearl Millet Cover Crop Extract Inhibits the Development of the Weed Ipomoea grandifolia by Inducing Oxidative Stress in Primary Roots and Affecting Photosynthesis Efficiency

The cover crop Pennisetum glaucum (L.) R.Br. (pearl millet) reduces the emergence of weed species in the field through a mechanism that is not fully known. The identification of the allelopathic activity of pearl millet can contribute to the development of no-tillage techniques to produce crops without or with low doses of herbicides. This issue was investigated by testing the effects of extracts from the aerial parts of pearl millet on the germination and growth of the weeds Bidens pilosa L., Euphorbia heterophylla L., and Ipomoea grandifolia (Dammer) O’Donell under laboratory conditions. The ethyl acetate fraction (EAF) at a concentration of 2000 µg mL−1 was inactive on Bidens pilosa; it inhibited root length (−72%) and seedling fresh weight (−41%) of E. heterophylla, and in I. grandifolia the length of primary root and aerial parts and the fresh and dry weight of seedlings were reduced by 63%, 32%, 25%, and 12%, respectively. In roots of I. grandifolia seedlings, at the initial development stage, EAF induced oxidative stress and increased electrolyte leakage. At the juvenile vegetative stage, a lower concentration of EAF (250 µg mL−1) induced a stimulus in seedling growth (+60% in root length and +23% in aerial parts length) that was associated with increased photosynthetic efficiency. However, at higher concentrations (1000 µg mL−1), it induced the opposite effects, inhibiting the growth of root (−41%) and aerial parts (−25%), with reduced superoxide dismutase activity and photosynthetic efficiency. The stilbenoid pallidol was identified as the main compound in EAF. The allelopathic activity of pearl millet may be attributed, at least in part, to the impairment of energy metabolism and the induction of oxidative stress in weed seedlings, with pallidol possibly involved in this action. Such findings demonstrated that the application of the EAF extract from pearl millet can be a natural and renewable alternative tool for weed control.

Zebrafish and Drosophila as Model Systems for Studying the Impact of Microplastics and Nanoplastics ‐ A Systematic Review

ABSTRACTMicroplastics and nanoplastics (MNPs) are byproducts of plastics created to benefit humanity, but improper disposal and inadequate recycling have turned them into a global menace that we can no longer conceal. As they interact with all living organisms, including humans, their mechanism of interaction and their perilous impact must be meticulously investigated. To uncover the secrets of MNPs, there must be model systems that exist to interlink the two major scenarios: they must represent the environmental impact and be relevant to humans. Therefore, zebrafish and Drosophila are perfect to describe these two cases, as they are well studied and relatable to humans. In this review, 39% zebrafish studies reported higher mortality and hatching rates at greater MNP concentrations, severe oxidative stress as seen by raised malondialdehyde (MDA) levels, and reduced superoxide dismutase (SOD) activity. About 50% of studies showed severe neurotoxic behavior with drop of locomotor activity, suggesting neurotoxicity. MNPs have a significant impact on fertility rate of Drosophila. More than half of the studies revealed genotoxicity in Drosophila as observed by wing spot assays and modified genomic expressions associated with stress and detoxification processes. These findings emphasize the potential of MNPs to bioaccumulate, impair physiological systems, and cause oxidative and neurobehavioral damage. This study underscores the importance for thorough risk evaluations of MNPs and their environmental and health consequences.

Maternal swimming with overload allied to postnatal high-fat, high-sugar diet induce subtle impairment on rat offspring's ovarian redox homeostasis.

Context The Developmental Origins of Health and Disease (DOHaD) concept suggests that early-life interventions significantly influence the long-term health outcomes of offspring. Emerging evidence supports that maternal physical exercise and balanced nutrition can positively impact the health of the next generation. Aims This study investigated the effects of maternal swimming combined with postnatal high-fat, high-sugar (HFHS) diet on the ovarian health of adult female Wistar rat offspring. Methods Adult female Wistar rats performed swimming exercise in a controlled temperature environment (32°C, 2% bodyweight overload adjusted daily) during 4weeks, starting 1week prior mating. The female offspring received a control or HFHS diet from postnatal day (PND) 21 to PND 90. We analyzed offspring's body weight, ovarian histomorphology, redox status, and associated molecular pathways 5' adenosine monophosphate-activated protein kinase (AMPKα), forkhead box O3 (FoxO3), and mitofusin 1 (Mfn-1). Key results Our findings reveal that maternal swimming exerted an effect on offspring body weight gain, delaying it. Individually, maternal exercise reduced superoxide dismutase (SOD) activity and mitofusin-1 levels, while the postnatal HFHS diet alone decreased both SOD and glutathione peroxidase (GPx) activities and increased the pFOXO3a/FOXO3a ratio in the ovaries. Conclusions We showed that combination of maternal swimming with a 2% overload and a postnatal HFHS diet can negatively affect the ovarian redox balance in offspring. Implications Prenatal and postnatal lifestyle might affect reproductive function in females.

Liquid mosquito repellent induces toxic effects in zebrafish.

Mosquitoes serve as vectors for life-threatening parasitic diseases, presenting a continuous threat throughout human history. This has resulted in the extensive utilization of various mosquito repellents, including liquid mosquito repellents (LMRs), roll-ons, and topical creams. While these products demonstrate significant efficacy, the toxicological implications associated with their use are not yet fully understood and continue to be a subject of debate. The analysis conducted using gas chromatography-mass spectrometry (GC-MS) on LMR revealed the presence of 158 distinct compounds, among which were Piperazine 2,5-dimethyl propyl and a range of hydrocarbons. The analysis of network toxicology indicated that 78 of the examined compounds contravened Lipinski's rule of five and exhibited considerable overlap with target genes associated with lung cancer pathways, thereby highlighting potential concerns regarding their carcinogenic properties. The exposure of zebrafish embryos to LMR concentrations between 0.1 and 14 µg/mL resulted in developmental toxicity assays that demonstrated a dose-dependent escalation in mortality rates and the occurrence of morphological abnormalities, such as pericardial edema and skeletal deformities. Behavioral assays demonstrated a marked decrease in locomotor activity at elevated LMR concentrations, indicating potential neurotoxic effects. Biochemical analyses revealed elevated levels of reactive oxygen species (ROS), enhanced lipid peroxidation, and diminished glutathione, which are indicative of oxidative stress. Enzyme activity assays indicated a reduction in superoxide dismutase (SOD) and catalase (CAT) activities, alongside an increase in lactate dehydrogenase (LDH) activity, which suggests the occurrence of cellular damage. Analysis of gene expression demonstrated significant dysregulation in genes associated with oxidative stress (SOD1, CAT), inflammatory markers (TNF-α, IL-1β), apoptotic regulators (p53, bcl2), and neurobiological genes (brain-derived neurotrophic factor, bdnf). The results highlight the possible health hazards linked to LMR exposure, which manifest as developmental, biochemical, and genetic alterations in zebrafish embryos.

Oxidative stress and apoptosis of the spinal cord in a rat model of retinoic acid-induced neural tube defects.

Neural tube defects (NTDs) are severe congenital anomalies that significantly impact the central nervous system, arising from the neural tube's failure to close during early embryogenesis. In this study, we investigated NTDs and associated pathophysiological mechanisms in foetal rats following exposure to all-trans retinoic acid (atRA). Out of 168 embryos from 15 pregnant rats in the experimental group, 78% displayed NTDs with notable spinal deformities, primarily in the lumbar-sacral region, similar to human cases. Body weight and crown-rump length (CRL) measurements indicated significant growth impairment in the NTD group compared to controls, while the atRA-treated group without NTDs showed no notable differences in growth. Immunohistochemistry (IHC) results demonstrated decreased NeuN and PCNA expression in the NTD group's spinal cord. Oxidative stress markers showed markedly reduced superoxide dismutase (SOD) and glutathione peroxidase (GSH-px) activity, alongside increased malondialdehyde (MDA) levels in the NTD group, indicating heightened oxidative stress. Analysis of apoptosis-related proteins revealed elevated Bax and caspase-3 levels, reduced Bcl-2 and lower poly (ADP-ribose) polymerase (PARP) in the NTD group, suggesting a pronounced shift towards proapoptotic pathways, potentially contributing to NTD progression. Our findings indicate that oxidative stress and apoptosis play significant roles in the development of NTDs. Future investigations should aim to pinpoint critical regulatory genes or proteins that might be targeted for therapeutic interventions to alleviate oxidative stress and apoptosis in NTD development.

Genetic analyses reveal wildfire particulates as environmental pollutants rather than nutrient sources for corals.

Heterotrophic nutrients are crucial for coral growth and recovery from bleaching events. Although wildfire emissions are a potential source of these nutrients, their impact on corals was minimally investigated. In this microcosm experiment, Acropora formosa corals exhibited rapid tissue detachment upon exposure to wildfire fine particulate matter (PM2.5). Physiological and genetic analyses revealed mechanisms associated with oxidation-reduction homeostasis and nutrient metabolism. Excessive hydrogen peroxide was generated as corals activated cytochrome P450 enzymes and the respiratory burst in phagocytic cells to metabolize PM2.5, leading to oxidative damage, mitochondrial dysfunction, and cell apoptosis due to reduced superoxide dismutase activity and compromised glutathione antioxidant function. Subsequently, corals upregulated the transcriptions of genes which are related to tyrosine receptor proteins to regulate multicellular development for self-repair, increasing energy consumption. However, Symbiodiniaceae upregulated their metabolism and retained photosynthates, reducing nutrient supply to the coral host. Therefore, the host temporarily utilized lipid reserves via the glyoxylate cycle, but excessive consumption disrupted lipid and carbohydrate metabolism, ultimately weakening cell adhesion and causing coral tissue detachment. Additionally, the downregulation of HSP70 expression, potentially linked to decreased sacsin and mitochondrial apoptosis, accelerated coral heat bleaching. This study elucidates the mechanisms by which wildfire PM2.5 at environmental concentrations poses risks to corals, particularly in a warming climate.

Roflumilast mitigates cisplatin-induced nephrotoxicity by regulating TNF-α/TNFR1/TNFR2/Fas/Caspase mediated apoptosis and inflammatory signals.

The study aimed to evaluate the effect of roflumilast on modulating TNF-α/Caspase mediated cellular signals in cisplatin-induced nephrotoxicity in rats. The rats (Male Wistar) were divided into five groups: normal control, disease control (cisplatin: 7mg/kg i.p.), and cisplatin + roflumilast (0.25, 0.5, and 1mg/kg b.w., p.o.). Cisplatin was administrated to rats on 0 day, and roflumilast treatment was started from the 6th-15th days. Blood and tissue were collected. Tissue was used to measure oxidative stress, such as malondialdehyde, superoxide dismutase, and catalase. Gene expression study involved real-time PCR of key genes linked with inflammation and apoptosis, i.e. Tnf-α, Tnfr1, Tnfr2, Fas, Nfkb, Casp3, Casp8, and Nrf2. Cisplatin showed decreased serum creatinine and urea, high albumin, and total protein. Cisplatin elevated the malondialdehyde and reduced superoxide dismutase and catalase activity. Cisplatin also attributed an overexpression of Tnf-α, Tnfr1, Tnfr2, Nfkb, Fas, Casp3, and Casp8, and a decrease in the Nrf2 gene. Roflumilast decreased creatinine and urea and increased albumin and total protein levels. Roflumilast also downregulated the expression of Tnf-α, Tnfr1, Tnfr2, Nfkb, Fas, Casp3, and Casp8 and upregulated the Nrf2 gene expression. Roflumilast manifested as a potential reno-protective agent against cisplatin-induced nephrotoxicity.

In-vitro and in-vivo assessment of the bactericidal potential of peracetic acid and hydrogen peroxide disinfectants against A. hydrophila infection in Nile tilapia and their effect on water quality indices and fish stress biomarkers

This study aimed to assess the in vitro and in vivo disinfectant potential of peracetic acid (PAA) (1 mg/L) and hydrogen peroxide (H2O2) (20 mg/L) on the physicochemical and microbiological water quality parameters of fish aquaria, the microbial density of Nile tilapia muscular tissue, fish hepatic cortisol levels, and antioxidant biomarkers. In vitro, PAA and H2O2 reduced A. hydrophila colony viability by 5 log units after 30 and 5 min of contact time, respectively. PAA and H2O2 were added to aquaria water twice a week for the three-week experiment. Increased fish escape reflexes were observed only in the PAA group, which returned to normal within 10 min. No mortalities were reported in either the PAA or H2O2 groups. An in vivo experimental challenge with a pathogenic strain of A. hydrophila revealed a 20% reduction in mortality in the PAA group, with no mortalities in the H2O2 group. Cortisol levels and antioxidant markers were measured to assess the impact of PAA and H2O2 on fish health. Cortisol levels in the PAA and H2O2 groups were significantly higher than in the control group after disinfectant exposure, but they progressively returned to normal. A significant reduction in superoxide dismutase (SOD) and catalase (CAT) activity, along with considerably higher glutathione peroxidase (GPx) and malondialdehyde (MDA) enzymatic activity, was observed in the PAA and H2O2 groups compared to the control group. A substantial increase in total antioxidant capacity (TAC) was recorded in the PAA group. Physicochemical analyses revealed reduced pH and increased dissolved oxygen levels in the PAA and H2O2 groups. Microbiological analyses showed a significant reduction in bacterial density in water by 64% and 76% after 30 min of exposure to PAA and H2O2, respectively, with a non-significant increase in microbial count after bacterial challenge. Additionally, aerobic bacterial count, Aeromonas spp., and psychotropic bacterial count in fish muscle showed a significant reduction in the H2O2 group compared to the PAA and control groups before and after infection. The study concludes that regular application of PAA and H2O2 can temporarily reduce bacterial load in aquaria and fish muscle, regulate stress responses, and improve fish health by reducing A. hydrophila-induced infections and improving survival.

The Inhibition of Reactive Oxygen Species Modulator 1 Attenuates Sevoflurane-Induced Neural Injury via Reducing Apoptosis and Oxidative Stress.

Sevoflurane causes neural injury by promoting apoptosis and oxidative stress. Reactive oxygen species modulator 1 (ROMO1) regulates apoptosis and oxidative stress, while its role in sevoflurane-induced neural injury remains unclear. This study intended to investigate the effect of ROMO1 knockdown on viability, apoptosis, and oxidative stress in sevoflurane-treated HT22 cells and its downstream pathway. HT22 cells were untreated (blank control), or treated with 1%, 2%, and 4% sevoflurane, respectively. Moreover, HT22 cells were transfected with siROMO1 small interfering RNA (siROMO1) or negative control siRNA (siNC) and then stimulated with 4% sevoflurane for further assays. Sevoflurane dose-dependently decreased cell viability and increased apoptosis rate versus blank control in HT22 cells. Sevoflurane elevated reactive oxygen species (ROS) fluorescence intensity, malondialdehyde (MDA), and lactate dehydrogenase (LDH) release, while reducing superoxide dismutase (SOD) activity in a dose-dependent manner versus blank control in HT22 cells. It also dose-dependently increased the relative mRNA and protein expressions of ROMO1 versus blank treatment in HT22 cells. Moreover, siROMO1 plus 4% sevoflurane increased cell viability, while decreasing apoptosis rate, ROS fluorescence intensity, MDA, and LDH release versus siNC plus 4% sevoflurane in HT22 cells. siROMO1 plus 4% sevoflurane elevated the phosphorylation of protein kinase B (AKT) versus siNC plus 4% sevoflurane in HT22 cells. ROMO1 inhibition reverses sevoflurane-induced neural injury by reducing apoptosis and oxidative stress in HT22 cells. The results indicate that ROMO1 may be a potential target for the management of sevoflurane-induced neural injury.

Molecular mechanisms of Buqing granule for the treatment of diabetic retinopathy: Network pharmacology analysis and experimental validation.

Diabetic retinopathy (DR) is a common microvascular complication of diabetes mellitus. Its blindness rate is high; therefore, finding a reasonable and safe treatment plan to prevent and control DR is crucial. Currently, there are abundant and diverse research results on the treatment of DR by Chinese medicine Traditional Chinese medicine compounds are potentially advantageous for DR prevention and treatment because of its safe and effective therapeutic effects. To investigate the effects of Buqing granule (BQKL) on DR and its mechanism from a systemic perspective and at the molecular level by combining network pharmacology and in vivo experiments. This study collected information on the drug targets of BQKL and the therapeutic targets of DR for intersecting target gene analysis and protein-protein interactions (PPI), identified various biological pathways related to DR treatment by BQKL through Gene Ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analyses, and preliminarily validated the screened core targets by molecular docking. Furthermore, we constructed a diabetic rat model with a high-fat and high-sugar diet and intraperitoneal streptozotocin injection, and administered the appropriate drugs for 12 weeks after the model was successfully induced. Body mass and fasting blood glucose and lipid levels were measured, and pathological changes in retinal tissue were detected by hematoxylin and eosin staining. ELISA was used to detect the oxidative stress index expression in serum and retinal tissue, and immunohistochemistry, real-time quantitative reverse transcription PCR, and western blotting were used to verify the changes in the expression of core targets. Six potential therapeutic targets of BQKL for DR treatment, including Caspase-3, c-Jun, TP53, AKT1, MAPK1, and MAPK3, were screened using PPI. Enrichment analysis indicated that the MAPK signaling pathway might be the core target pathway of BQKL in DR treatment. Molecular docking prediction indicated that BQKL stably bound to these core targets. In vivo experiments have shown that compared with those in the Control group, rats in the Model group had statistically significant (P < 0.05) severe retinal histopathological damage; elevated blood glucose, lipid, and malondialdehyde (MDA) levels; increased Caspase-3, c-Jun, and TP53 protein expression; and reduced superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) levels, ganglion cell number, AKT1, MAPK1, and MAPK3 protein expression. Compared with the Model group, BQKL group had reduced histopathological retinal damage and the expression of blood glucose and lipids, MDA level, Caspase-3, c-Jun and TP53 proteins were reduced, while the expression of SOD, GSH-Px level, the number of ganglion cells, AKT1, MAPK1, and MAPK3 proteins were elevated. These differences were statistically significant (P < 0.05). BQKL can delay DR onset and progression by attenuating oxidative stress and inflammatory responses and regulating Caspase-3, c-Jun, TP53, AKT1, MAPK1, and MAPK3 proteins in the MAPK signaling pathway mediates these alterations.

Nebivolol prevents redox imbalance and attenuates bladder dysfunction induced by cyclophosphamide in mice.

Cyclophosphamide (CYP) is combined with cytoprotective agents to minimize its toxicity in the bladder, which is mediated by reactive oxygen species (ROS). Using multiple antioxidant mechanisms, nebivolol protects from oxidative stress in distinctive conditions. We hypothesized that nebivolol would attenuate both molecular and functional alterations induced by CYP in the bladder. Male C57BL/6 were pretreated or not with nebivolol (10mg/kg/day, gavage), which was given 5 days before a single injection of CYP (300mg/kg; i.p.). Molecular and functional parameters were assessed at 24h in the bladder. Nebivolol prevented increases in ROS generation and lipoperoxidation as well as reduction of superoxide dismutase activity induced by CYP. Increased voiding frequency, decreased voiding interval, and reduced bladder capacity were found in CYP-treated mice. These responses were prevented by nebivolol. An augmented number of urinary spots and smaller urinary volumes were detected in CYP-injected mice, and nebivolol partially prevented these responses. The reduction of ROS levels is the primary mechanism by which nebivolol attenuates the deleterious effects of CYP in the bladder. The association of nebivolol with other cytoprotective agents could be an option to prevent CYP-associated oxidative damage to the bladder during chemotherapy.

Upregulation of Mitochondrial Sirt3 and Alleviation of the Inflammatory Phenotype in Macrophages by Estrogen.

Aging and comorbidities like type 2 diabetes and obesity contribute to the development of chronic systemic inflammation, which impacts the development of heart failure and vascular disease. Increasing evidence suggests a role of pro-inflammatory M1 macrophages in chronic inflammation. A shift of metabolism from mitochondrial oxidation to glycolysis is essential for the activation of the pro-inflammatory M1 phenotype. Thus, reprogramming the macrophage metabolism may alleviate the pro-inflammatory phenotype and protect against cardiovascular diseases. In the present study, we hypothesized that the activation of estrogen receptors leads to the elevation of the mitochondrial deacetylase Sirt3, which supports mitochondrial function and mitigates the pro-inflammatory phenotype in macrophages. Experiments were performed using the mouse macrophage cell line RAW264.7, as well as primary male or female murine bone marrow macrophages (BMMs). Macrophages were treated for 24 h with estradiol (E2) or vehicle (dextrin). The effect of E2 on Sirt3 expression was investigated in pro-inflammatory M1, anti-inflammatory/immunoregulatory M2, and naïve M0 macrophages. Mitochondrial respiration was measured by Seahorse assay, and protein expression and acetylation were determined by western blotting. E2 treatment upregulated mitochondrial Sirt3, reduced mitochondrial protein acetylation, and increased basal mitochondrial respiration in naïve RAW264.7 macrophages. Similar effects on Sirt3 expression and mitochondrial protein acetylation were observed in primary female but not in male murine BMMs. Although E2 upregulated Sirt3 in naïve M0, pro-inflammatory M1, and anti-inflammatory/immunoregulatory M2 macrophages, it reduced superoxide dismutase 2 acetylation and suppressed mitochondrial reactive oxygen species formation only in pro-inflammatory M1 macrophages. E2 alleviated the pro-inflammatory phenotype in M1 RAW264.7 cells. The study suggests that E2 treatment upregulates Sirt3 expression in macrophages. In primary BMMs, female-specific Sirt3 upregulation was observed. The Sirt3 upregulation was accompanied by mitochondrial protein deacetylation and the alleviation of the oxidative and pro-inflammatory phenotype in M1 macrophages. Thus, the E2-Sirt3 axis might be used in a therapeutic strategy to fight chronic systemic inflammation and prevent the development of inflammation-linked diseases.

Pera orange juice (Citrus sinensis L. Osbeck) alters lipid metabolism and attenuates oxidative stress in the heart and liver of rats treated with doxorubicin

BackgroundDoxorubicin (DOX) is a highly effective chemotherapy drug widely used to treat cancer, but its use is limited due to multisystemic toxicity. Lipid metabolism is also affected by doxorubicin. Orange juice can reduce dyslipidemia in other clinical situations and has already been shown to attenuate cardiotoxicity. Our aim is to evaluate the effects of Pera orange juice (Citrus sinensis L. Osbeck) on mitigating lipid metabolism imbalance, metabolic pathways, and DOX induced cytotoxic effects in the heart and liver. MethodsTwenty-four male Wistar rats were allocated into 3 groups: Control (C); DOX (D); and DOX plus Pera orange juice (DOJ). DOJ received orange juice for 4 weeks, while C and D received water. At the end of each week, D and DOJ groups received 4 mg/kg/week DOX, intraperitoneal. At the end of 4 weeks animals were submitted to echocardiography and euthanasia. ResultsAnimals treated with DOX decreased water intake and lost weight over time. At echocardiography, DOX treated rats presented morphologic alterations in the heart. DOX increased aspartate aminotransferase (AST), alanine aminotransferase (ALT), total cholesterol, high density lipoprotein (HDL), low-density lipoprotein (LDL), and triglycerides. It also reduced superoxide dismutase (SOD) activity, increased protein carbonylation in the heart and dihydroethidium (DHE) expression in the liver, decreased glucose transporter type 4 (GLUT4) and the nuclear receptor peroxisome proliferator-activated receptor γ (PPARγ1) in the heart, and reduced carnitine palmitoyltransferase I (CPT1) in the liver. ConclusionDOX caused dyslipidemia, liver and cardiac toxicity by increasing oxidative stress, and altered energy metabolic parameters in both organs. Despite not improving changes in left ventricular morphology, orange juice did attenuate oxidative stress and mitigate the metabolic effects of DOX.

Ameliorative Potential of Ginger for Mitigating Liver Damage Caused by Fluopyram in Male Albino Rats

Fluopyram is a widely used new generation broad spectrum fungicide and a variety of biochemical and histopathological alterations in the livers of albino rats. These include inflammatory cells, dilated sinusoids, haemorrhage, dilation of central veins, congestion and presence of erythrocytes. Significant increase in blood alanine aminotransferase (ALT), aspartate amino transferase (AST), acid phosphatise (ACP) and decrease in alkaline phosphatise (AKP) enzyme levels were seen in high dose of fluopyram treated rats as compared to control. The oxidative stress and antioxidant enzymes showed a significant reduction in superoxide dismutase (SOD), catalase (CAT) and increase in malondialdehyde (MDA) level. Rats treated with fluopyram and ginger showed improved histopathological changes in liver. Ginger extract also showed decreased serum levels of malondialdehyde and raised serum levels of antioxidant enzymes. According to the current study, strong antioxidant activity of ginger mediates its protective effect against fluopyram induced liver damage.

Anticoccidial and Antioxidant Activities of an Ethanolic Extract of Teucrium polium Leaves on Eimeria papillate-Infected Mice.

Eimeria spp. are responsible for the economic loss of both domestic and wild animals due to coccidiosis, the most common parasitic disease. The resistance to currently available drugs used to treat coccidiosis has been proven. Medicinal plants that contain physiologically active phytochemicals have been widely used in traditional medicine. Teucrium polium leaf extract (TPLE) has been shown to exhibit pharmacological, antioxidant, and anticoccidial properties in different experiments. Here, our investigation focused on how T. polium leaf extract affected the way that Eimeria papillate caused intestinal injury in mice. Thirty-five male Swiss albino mice were divided into seven groups, as follows: group I: untreated and uninfected (negative control); group II: uninfected, treated group with TPLE (150 mg/kg b.w); and group III: infected untreated (positive control). Groups III-VII were orally administered 103 sporulated E. papillata oocysts. A total of 60 min after infection, groups IV-VI were treated for five successive days with 50, 150, and 250 mg/kg b.w TPLE, respectively, while group VII was treated with amprolium (120 mg/kg b.w.). The mice had been euthanized on the fifth day post-infection, and the jejunum tissues were prepared for histology and oxidative stress studies. A total of 150 mg/kg of TPLE was the most effective dosage, significantly decreasing oocyst output by about 80.5%, accompanied by a significant reduction in the number of developmental parasitic phases in jejunal sections. In addition, the decrease in the number of goblet cells in the jejuna of mice raised after treatment. Also, TPLE greatly diminished the body weight loss of infected mice. Moreover, our research proved that TPLE reduced oxidative damage due to E. papillata infection via decreasing intestinal malondialdehyde (MDA) and nitric oxide (NO) levels and increasing reduced superoxide dismutase (SOD) and glutathione (GSH) levels. These results demonstrated that TPLE had potent anticoccidial properties. TPE's efficacy as a natural antioxidant has also been demonstrated in reducing oxidative stress and enhancing antioxidant systems to mitigate biochemical and histological changes in the jejunum caused by E. papillata.

From Personal Care to Coastal Concerns: Investigating Polyethylene Glycol Impact on Mussel's Antioxidant, Physiological, and Cellular Responses.

Pharmaceutical and personal care products (PPCPs) containing persistent and potentially hazardous substances have garnered attention for their ubiquitous presence in natural environments. This study investigated the impact of polyethylene glycol (PEG), a common PPCP component, on Mytilus galloprovincialis. Mussels were subjected to two PEG concentrations (E1: 0.1 mg/L and E2: 10 mg/L) over 14 days. Oxidative stress markers in both gills and digestive glands were evaluated; cytotoxicity assays were performed on haemolymph and digestive gland cells. Additionally, cell volume regulation (RVD assay) was investigated to assess physiological PEG-induced alterations. In the gills, PEG reduced superoxide dismutase (SOD) activity and increased lipid peroxidation (LPO) at E1. In the digestive gland, only LPO was influenced, while SOD activity and oxidatively modified proteins (OMPs) were unaltered. A significant decrease in cell viability was observed, particularly at E2. Additionally, the RVD assay revealed disruptions in the cells subjected to E2. These findings underscore the effects of PEG exposure on M. galloprovincialis. They are open to further investigations to clarify the environmental implications of PPCPs and the possibility of exploring safer alternatives.

Effects of far-red light on growth, endogenous hormones, antioxidant capacity and quality of Lettuce

This study aimed to explore the effects of various intensities of far-red light on the growth performance, endogenous hormones, antioxidant indices, and overall quality of hydroponically cultivated lettuce. As the control treatment, a white LED emitting light at an intensity of 200 µmol/(m2·s) was utilized (referred to as CK with an R/FR ratio of 5.5), while two experimental treatments, FT1 (R/FR = 1.2) and FT2 (R/FR = 0.8), were established by adding different intensities of far-red light to the CK treatment. The results demonstrated that the application of far-red light, particularly in FT1, led to a significant increase in plant height, leaf area, and lettuce biomass, while simultaneously resulting in a notable reduction in leaf thickness. The content of indole-3-acetic acid (IAA) and abscisic acid (ABA) in response to far-red light treatments exhibited an initial increase followed by a subsequent decrease, with FT2 experiencing a significant decline. The gibberellin (GA3) content in FT2 reached its peak on the 35th day, showing a substantial increase of 60.09% compared to CK. Far-red treatments were found to enhance peroxidase (POD) and catalase (CAT) activities, while significantly reducing superoxide dismutase (SOD) activity. In comparison to CK, FT1 exhibited a remarkable 134.33% increase in anthocyanin content. Both FT1 and FT2 significantly boosted vitamin C levels while reducing nitrite content. Additionally, the application of far-red light treatment significantly increased the alcohol and ester content in lettuce leaves. This study establishes a theoretical foundation for enhancing the quality and flavor of lettuce using different far-red light treatments.Graphical

Renal denervation ameliorated salt-induced hypertension by improving cardiac work, cardiac enzyme and oxidative balance in Sprague-Dawley rats

BackgroundHypertension is associated with cardiovascular dysfunction, dysregulation of the antioxidant system and alteration of the level of some enzymes in the metabolic pathway. The possible modulatory effect of acute renal denervation (ARD) on cardiovascular function and the antioxidant system is still a subject of intense debate. This study sought to ascertain the ameliorative effects of ARD on cardiovascular parameters, antioxidant system, creatine kinase and lactate dehydrogenase levels. MethodsThirty-six Sprague-Dawley rats (5–6 weeks old) were divided into 6 groups of 6 animals each consisting of Normal Salt, High Salt, Normal Salt + Sham Denervation, High Salt + Sham Denervation, Normal Salt + Renal Denervation and High Salt + Renal Denervation. Induction of hypertension with 8 % salt in the diet lasted for 8 weeks. Renal or Sham denervation was thereafter done on selected groups. At the end of the experimental period, cardiovascular parameters, plasma antioxidant status, plasma creatine kinase (CK) and lactate dehydrogenase (LDH) levels were assessed. Significance level was set at p < 0.05. ResultsSalt-loading significantly increased systolic blood pressure (SBP), diastolic blood pressure (DBP), mean arterial blood pressure (MABP), rate pressure product (RPP) while reducing superoxide dismutase (SOD), reduced glutathione (GSH) and catalase (CAT). Acute renal denervation significantly (p < 0.0001) reduced SBP, DBP, MABP, RPP, LDH and norepinephrine level while increasing SOD, GSH and CAT. ARD did not significantly alter CK level. ConclusionAcute renal denervation, by reducing sympathetic activity, ameliorates cardiovascular and antioxidant functions as well as reduces LDH level without significantly altering CK level in salt-induced hypertension.

Effect of Sodium Fluoride on Oxidative Stress and Antioxidant System in Male Wistar Rats

This research aimed to examine the effect of sodium fluoride (NaF) on oxidative stress and antioxidant systems in the serum, aorta, and cardiac tissues of male Wistar rats. The increased attention to sodium fluoride and its detrimental effects on human health in recent years has led to concerns. Excessive ingestion and accumulation of sodium fluoride from water, toothpaste, and pesticides could initiate oxidative stress in the blood, aorta, and heart. This heightened oxidative stress and disturbance in the antioxidant system pose a significant risk and may predispose the body to severe vascular and cardiovascular-related diseases, which are leading causes of global mortality. In this study, ten male Wistar rats weighing 150-180g were grouped into two (n=5). Group I Control received distilled water, and Group 2 received 10mg/kg NaF orally for 21 days. Markers of oxidative stress malondialdehyde (MDA) and reduced glutathione (GSH), antioxidant enzymes superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), and total antioxidant capacity (TAC) were measured in the serum, aorta, and heart. Data were analyzed using descriptive statistics of student t-test at α0.05. The data were presented as mean ± SEM. The oral administration of sodium fluoride resulted in an elevation of MDA levels in the serum, aorta, and heart of the rats exposed to NaF. Additionally, the oral administration of sodium fluoride led to a reduction in superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) levels in the serum, aorta, and heart of rats exposed to NaF. Furthermore, the oral administration of sodium fluoride resulted in a decrease in the total antioxidant capacity (TAC) in the serum, aorta, and heart of rats exposed to sodium fluoride. This study demonstrated that sodium fluoride exposure diminishes the antioxidant capacity in the serum, aorta, and heart, indicating that sodium fluoride exposure induces oxidative stress, potentially affecting the functions of the aorta and heart. Therefore, the continuous exposure to fluoride in populations residing in regions with endemic fluorosis worldwide should be a topic of considerable concern. This research work was self-funded. This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

Evaluation of the vascular and cardiac effects of treatment with copaiba oil and white pitch: a perspective for reducing oxidative stress and improving cardiac microstructure

Autism is a neuropsychiatric disorder that develops in childhood and may have associated comorbidities, such as heart disease. As a treatment, alternative therapy means are being sought to conventional methods. For study purposes, autism has been induced through gestational exposure to valproic acid. With the aim of evaluating the vascular and cardiac effects of treatment with copaiba essential oil and white pitch caused by gestational exposure to valproic acid, on the 13th day of pregnancy, the rats in the negative control group received water and those in the experimental groups received valproic acid (600 mg/kg), intraperitoneally, once. The male puppies were divided into six groups: negative and positive controls; vehicle; treated with copaiba oil; with white pitch oil and copaiba oil associated with white pitch. TERRA® oils were administered via gavage for 30 consecutive days. As a result, a reduction in superoxide dismutase, catalase and creatine kinase and an increase in total antioxidant activity and malondialdehyde were verified. Presence of myocarditis, vacuolation and necrosis of cardiomyocytes. There was no significant change in area and diameter, but there was an increase in the volume density and length of cardiomyocytes and a decrease in the volume density of blood vessels and interstices and the length density of blood vessels. Thus, exposure to valproic acid during the intrauterine period caused changes in the cardiac microstructure. However, the use of copaíba and white pitch essential oils led to oxidative and nitrosative stress, and the combination of the two oils has promising results in reversing this condition.