Glutathione Peroxidase Levels Research Articles

Evaluation of the sperm parameters, oxidative stress, and histopathological effects of vitamin B12 in preventing Helicobacter pylori-induced testicular toxicity: An experimental study.

Helicobacter pylori (H. pylori) causes sterility by affecting the reproductive system. Vitamin B12 improves sperm quantity and function. Vitamin B12 protection against H. pylori adverse effects was investigated. 40 C57 male mice (6 wk) were randomly assigned to 4 equal groups (n = 10) including, group 1 (control without any intervention), group 2 (H), 3 (HP), and 4 (HB) received 1 109 colony forming unit (CFU) of H. pylori, 1 109 CFU of H. pylori+phosphate buffered saline, 1 109 CFU of H. pylori+50 g/kg vitamin B intraperitoneally, respectively. In the induction groups, the H. pylori was orogasterically injected 3 times with 1 cc phosphate buffered saline throughout the day. Then testicular metrics, sperm motility, viability, quantity, and shape, plasma levels of malondialdehyde (MDA), superoxide dismutase, glutathione peroxidase, and total antioxidant capacity were measured. Also, testicular-tissue changes were examined using Johnson scores, tubular differentiation index, and spermatogenesis index. Vitamin B12, homocysteine, and testosterone serum levels were examined. The results showed a significantly lower Johnson score, tubular differentiation index, and spermatogenesis index, and serum level of testosterone and homocysteine as well as a higher MDA level in the H and HP groups than the HB group (p 0.05). In contrast, the highest superoxide dismutase and glutathione peroxidase enzymes activity and total antioxidant capacity as well as the lowest serum level of MDA were found in the HB group compared to other groups (p 0.05). Vitamin B increased antioxidant enzyme activity, enhanced sperm parameters, and decreased injury to testicular tissue. It can be used as a potent antioxidant in reducing testicular damage induced by H. pylori.

Metformin improves cognitive dysfunction through SIRT1/NLRP3 pathway-mediated neuroinflammation in db/db mice.

Diabetes mellitus (DM), an important public health problem, aggravates the global economic burden. Diabetic encephalopathy (DE) is a serious complication of DM in the central nervous system. Metformin has been proven to improve DE. However, the mechanism is still unclear. In this study, the db/db mice, a common model used for DE, were employed to explore and study the neuroprotective effect of metformin and related mechanisms. Behavioral tests indicated that metformin (100 or 200 mg/kg/day) could significantly improve the learning and memory abilities of db/db mice. The outcomes from the oral glucose tolerance test (OGTT) and insulin tolerance test (ITT) demonstrate that metformin effectively modulates glucose and insulin signaling pathways in db/db mice. The results of body weight and blood lipid panel (total cholesterol, triglycerides, high-density lipoprotein cholesterol, low-density lipoprotein cholesterol) show that metformin promotes the level of lipid metabolism in db/db mice. Furthermore, data from oxidative stress assays, which measured levels of malondialdehyde, superoxide dismutase, catalase, and glutathione peroxidase, suggest that metformin suppresses oxidative stress-induced brain damage in db/db mice. In addition, western blot, Nissl staining, and immunofluorescence results showed that metformin increased the expressions of nerve growth factor and postsynaptic density 95 and repaired neuronal structural damage. For the mechanism study, metformin activated SIRT1 and inhibited the expression of NLRP3 inflammasome (NLRP3, ASC, caspase-1, IL-1β, and IL-18) and inflammatory cytokines (TNFα and IL-6). In conclusion, metformin could ameliorate cognitive dysfunction through the SIRT1/NLRP3 pathway, which might be a promising mechanism for DE treatment.

Golgi protein ACBD3 downregulation sensitizes cells to ferroptosis.

Ferroptosis, a form of cell death driven by iron-dependent lipid peroxidation, is emerging as a promising target in cancer therapy. It is regulated by a network of molecules and pathways that modulate lipid metabolism, iron homeostasis and redox balance, and related processes. However, there are still numerous regulatory molecules intricately involved in ferroptosis that remain to be identified. Here, we indicated that suppression of Golgi protein acyl-coenzyme A binding domain A containing 3 (ACBD3) increased the sensitivity of Henrieta Lacks and PANC1 cells to ferroptosis. ACBD3 knockdown increases labile iron levels by promoting ferritinophagy. This increase in free iron, coupled with reduced levels of glutathione peroxidase 4 due to ACBD3 knockdown, leads to the accumulation of reactive oxygen species and lipid peroxides. Moreover, ACBD3 knockdown also results in elevated levels of polyunsaturated fatty acid-containing glycerophospholipids through mechanisms that remain to be elucidated. Furthermore, inhibition of ferrtinophagy in ACBD3 downregulated cells by knocking down the nuclear receptor co-activator 4 or Bafilomycin A1 treatment impeded ferroptosis. Collectively, our findings highlight the pivotal role of ACBD3 in governing cellular resistance to ferroptosis and suggest that pharmacological manipulation of ACBD3 levels is a promising strategy for cancer therapy.

Evaluation of the Possible Pathophysiological Role of Redox Status in Patients with Sickle Cell Anemia

Abstract BACKGROUND: The disease of sickle cell anemia (SCA) is an inherited blood disease that causes several complications, and oxidative stress (OS) may play a very important role in its complications and pathophysiology. OBJECTIVE: The aims of the study is to evaluate the possible pathophysiological role of some antioxidant and oxidant biomarkers within SCA patients and to evaluate the correlation of OS and atherogenic index of plasma (AIP) to predict the cardiovascular risk in SCA subjects. MATERIALS AND METHODS: A case–control research includes three study groups: SCA patients, sickle cell trait (SCT) subjects, and healthy controls (HCs). All study groups were evaluated for their serum catalase (CAT), serum superoxide dismutase (SOD), glutathione peroxidase (GPx), and malondialdehyde (MDA) as well as plasma triglycerides and high-density lipoprotein cholesterol. Data were collected, tabulated, and statistically analyzed using (SPSS) version 31 program. The frequencies, relative frequencies, and means were obtained as descriptive methods. The associations among parameters were obtained using the Chi-square statistical method. RESULTS: The results revealed significantly lower levels of serum SOD and GPx among sickle cell disease (SCD) and SCT subjects than the HCs, whereas the inverse findings were reported for CAT and AIP. However, the MDA results revealed a significantly higher level in SCD patients compared to SCT and HC. Furthermore, the levels of SOD and MDA were positively associated in all study groups, and the levels of GPx and MDA were negatively correlated in SCD and SCT groups. The AIP was positively correlated with MDA in the SCT group and negatively correlated with CAT in the SCD group. CONCLUSIONS: The conclusion of the study indicated the presence of an OS and antioxidant compensatory status in patients with SCD and the SCT subjects. The altered biomarkers in SCA patients made it clear that the impairment and generation of OS in this disease, as well as antioxidant biomarkers, are contributory factors toward cellular redox homeostasis. This addressed the aim of the study.

Effect of tangeretin on cisplatin-induced oxido-inflammatory brain damage in rats.

Cisplatin (CIS) is a platinum-derived chemotherapeutic agent commonly utilized in the treatment of various malignant tumours. However, anticancer doses of the drug cause serious damage to the brain. This study aimed to determine the potential protective effects of tangeretin, which has antioxidant and anti-inflammatory properties, in cisplatin-induced neurotoxicity on BALB/c mice brains. Male BALB/c mice were randomized and separated into four groups. Tangeretin was given for 10 days by gavage. CIS was injected as a single dose of 10 mg/kg intraperitoneally (ip) on the 10th day. Brain tissues, malondialdehyde (MDA), total glutathione (tGSH), glutathione peroxidase (GPx), superoxide dismutase (SOD), catalase (CAT) and nitric oxide (NO) levels were measured to determine oxidative damage and myeloperoxidase, tumour necrosis factor-alpha (TNF-α), interleukin 1 beta (IL-1β), IL-6 and IL-10 were measured to determine inflammatory activity. In addition, 8-OHdG and caspase-3 were analysed by immunofluorescence methods. While CIS administration remarkably elevated reactive oxygen species, MDA, and NO levels in brain tissue compared to the control, tGSH, GPx, SOD and CAT levels were significantly decreased. Also, it has been detected that TNF-α, IL-1β and IL-6 obtained in CIS-treated groups increased as well as IL-10 decreased, thereby elevating the inflammatory response. In addition, 8-OHdG and caspase-3 immunoreactivity in neurons increased with CIS administration. Treatment with tangeretin ameliorated the deterioration in oxidant/antioxidant status, overpowered neuroinflammation and ameliorated neurotoxicity-induced apoptosis. This study shows that tangeretin has beneficial effects on CIS-induced neurodegeneration. Possible mechanisms underlying these beneficial effects include the antioxidant and anti-inflammatory properties of tangeretin.

The Effect of Chronic Administration of Amphetamine-Type Stimulants on Oxidative Stress and Inflammation in Wistar Rats

تهدف هذه الدراسة إلى تحديد تأثير التناول المزمن للمنشطات من نوع الأمفيتامين بجرعات متفاوتة على الالتهاب والإجهاد التأكسدي في فئران ويستار. تم إعطاؤهم ميثيلفينيديت وتم تقسيمهم إلى 4 مجموعات علاجية. علاوة على ذلك ، تم إجراء تجميع عشوائي بسيط لتقسيم العينات إلى 5 مجموعات ، تتكون كل مجموعة من 9 فئران. تضمنت هذه المجموعات الفئران التي أعطيت فقط الماء المقطر كعناصر تحكم ، بالإضافة إلى تلك التي أعطيت ميثيلفينيديت بجرعات 10 مجم / كجم من وزن الجسم ، و 20 مجم / كجم من وزن الجسم ، و 40 مجم / كجم من وزن الجسم لمدة 4 أسابيع كمجموعات تجريبية. ثم تم إجراء التحليل الإحصائي باستخدام GraphPad Prism لمقارنة تأثيرات الإجهاد التأكسدي والالتهاب الجهازي و BDNF والذاكرة المكانية لفئران Wistar. أدى الاستخدام المزمن للمنشطات إلى انخفاض كبير في مستويات الجلوتاثيون بيروكسيديز وكذلك زيادة في إطلاق IL-6 وعامل نخر الورم ألفا مقارنة بمجموعة التحكم. بناءً على النتائج ، لعبت المسارات المتورطة في الضعف الإدراكي ، والتي كانت مرتبطة باستخدام المنشطات من نوع الأمفيتامين ، دورًا في معالجة التأثير الضار لتعاطي المخدرات والأمراض المصاحبة لها.

Ginger (Zingiber officinale) attenuates the neurotoxicity in rats induced by organophosphate pesticide

BackgroundWe are exposed to different chemicals in various ways in our daily life, and these can be toxic at minute concentrations. The pesticides used for different purposes are also toxic and may pose threat to life by inducing oxidative stress. Dichlorvos (DDVP) is an organophosphate pesticide used for various purposes and is also reported to be toxic. In this study, the neurotoxicity of DDVP exposure was studied. The role of ginger, Zingiber officinale (ZO), was also evaluated against the neurotoxic effects of DDVP. Forty-eight Wistar rats of both the sexes were used in this study. The rats were exposed to DDVP and post-treatment with ZO was given. The oxidative stress in terms of lipid peroxidation (LPO), reduced glutathione (GSH), catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPx), and glutathione reductase (GR) levels were estimated after exposure and treatment.ResultsDDVP resulted in oxidative stress, evidenced by enhanced LPO level. The simultaneous reductions in other non-enzymatic and enzymatic antioxidants were reported. The post-treatment with ZO led to a reduction in oxidative stress in rat brains. The levels of SOD, CAT, GSH, GR, and GPx were increased whereas declined levels of LPO were reported after treatment.ConclusionHence, ginger can help mitigate the pesticide toxicity through the up-regulation of antioxidant levels.

Transcriptomic analysis reveals nanoplastics-induced apoptosis, autophagy and immune response in Litopenaeus vannamei

Increasing attention is being paid to the toxic physiological effects of nanoplastics (NPs) on aquatic organisms. However, few studies have systematically evaluated the regulatory mechanisms of NPs on immune response in crustaceans. In this study, a 28-day chronic exposure experiment was conducted in which shrimps were exposed to various 80-nm polystyrene NPs concentrations (0, 0.1, 1, 5 and 10 mg/L). Transcriptomic analysis was used to investigate the regulatory mechanisms of NPs in immune response of Litopenaeus vannamei. With increasing NPs concentration, the total hemocyte count (THC) content decreased, while phagocytosis rate (PR) and respiratory burst (RB) showed trends of first rising and then falling. High concentration (10 mg/L) of NPs caused the destruction of hepatopancreas tissue structure, the shedding of microvilli, the increase number of hepatocyte apoptosis and autophagy structure. With increasing NPs concentration, the lysozyme (Lys), superoxide dismutase (SOD) and glutathione peroxidase (GPx) activities first increased and then decrease, while contents of lipid peroxidation and malondialdehyde increased; the expression levels of Toll, MyD88, GPx, SOD, proPO, Lys, and ALF generally increased at first and then decreased. Transcriptional sequencing analysis showed that the pathway of differentially expressed genes in KEGG enrichment mainly included lysosome (ko04142), apoptosis (ko04210) pathways, indicating that the NPs mainly affected the immune regulatory mechanism. Further analysis by Gene Set Enrichment Analysis (GSEA) showed that the up-regulation pathways of NPs activation mainly included immune response-related pathways such as mitochondrial autophagy, DNA repair, autophagosomes signaling pathway. Our results indicated that NPs exposure induced oxidative stress, apoptosis and autophagy in shrimps. This study provides a basis for further understanding of the mechanisms of antioxidant immune regulation by NPs in shrimp and may serve as a reference for healthy ecological culture of shrimp.

Fucoidan Inhibits Prostate Cancer Growth Through Modulation of Different Cell Deaths.

Docetaxel (DOC) is the main chemotherapeutic agent for the treatment of advanced metastatic prostate cancer. Docetaxel shows anticancer effects by preventing the depolymerization of microtubules in the cell, therefore preventing cell division. However, the low survival effect of docetaxel has prompted researchers to search for novel therapeutic agents. Fucoidan (FUC) is a sulfated polysaccharide derived from brown algae. It has many bioactivities which makes fucoidan a promising anticancer agent. In this study, the potential anti-tumorigenic and preventive effects of fucoidan with or without docetaxel in prostate cancer were investigated by analyzing different cell death modalities. The in-vivo six groups (n = 8) were conducted; preventive (Pt), docetaxel treated after preventive (Pt-D), control, fucoidan (FUC), docetaxel (DOC), and FUC and DOC (FUC+DOC) combination. Apoptotic, necroptotic, and autophagic cell death-related protein expressions were assessed in tumor tissues by using immunohistochemical staining. Oxidative stress-related lipid peroxidation, glutathione peroxidase, and glutathione levels were also determined in tumor tissues. Although apoptotic, necroptotic, and autophagic cell deaths were significantly induced in agent-treated groups compared to the control. Apoptotic cell death was more significantly induced in FUC and FUC+DOC-treated groups. Necroptotic cell death was increased considerably by inducing MLKL protein expression in all treatment groups. In the FUC, Pt, and DOC groups, LC3A/B expressions were significantly increased. DOC, FUC+DOC, and Pt-D treatments caused a significant increase in Beclin-1 expression. Oxidative stress-related MDA, GPX, and GSH levels significantly decreased with FUC treatment. The anti-tumorigenic effects of FUC and DOC were also demonstrated through tumor size reduction. According to the findings of this study, FUC inhibited tumor growth temporally and dimensionally, especially in preventive applications. FUC and FUC+DOC combinations in both treatment groups showed anti-tumorigenic effects. The results of this study suggest that fucoidan is a promising anticancer agent against prostate cancer. FUC can be considered as a preventive or treatment agent in prostate cancer therapy with DOC. Further studies are needed to fully elucidate the mechanism of action of fucoidan in metastatic prostate cancer.

Effect of berberine on the hippocampal structure, biochemical factors, memory, and blood-brain barrier in rat model of transient global cerebral ischemia.

Global cerebral ischemia (GCI) results in damage to the neurons and leads to cognitive impairments. Berberine (BBR) is known for its neuroprotective qualities. This study aimed to investigate the effects of BBR on memory, Blood-brain barrier (BBB) permeability, biochemical factors, and neuronal structure. Sixty-three adult male Wistar rats were divided randomly into Sham (21), GCI (21), and GCI + BBR (21) groups. The GCI + BBR group received 50 mg/kg of BBR for 7 days before and 6 h after 20 min of GCI induction. After 24 h, assessments included hippocampal neuronal structure, catalase (CAT), superoxide dismutase (SOD), malondialdehyde (MDA), and glutathione peroxidase (GPX) levels, memory performance, and BBB permeability. The GCI + BBR group reduced volume loss in the CA1 and its sublayers (oriens, pyramidal, and radiatum) compared to the GCI group (p < 0.0001, p < 0.001, p < 0.01 and p < 0.001, respectively). Additionally, the GCI + BBR group showed higher pyramidal neuron density (p < 0.0001) and number (p < 0.0001) compared to the GCI group. BBR also decreased MDA levels (p < 0.0001) and increased CAT activity (p < 0.0001) in the GCI + BBR group compared to the GCI group, with GPX and SOD activity approaching Sham levels (p < 0.0001, both). BBR demonstrated significant improvements in short and long-term memory compared to the GCI group (p < 0.01, p < 0.0001, respectively). Furthermore, BBB permeability in the GCI + BBR group was significantly reduced compared to the GCI group (p < 0.0001). These findings demonstrated BBR's potential to protect the neurons in the CA1 and BBB structures, enhance antioxidant activity, and alleviate GCI-induced memory impairments.

Astragalus polysaccharide alleviates IL-13-induced oxidative stress injury in nasal epithelial cells by inhibiting WTAP-mediated FBXW7 m6A modification

Abstract Background Allergic rhinitis (AR) a common and complicated upper airway disease mediated by specific IgE antibodies. Our study aims to explore the pharmacological effects of astragalus polysaccharide (APS) on AR and elucidate the mechanisms involved. Methods RT-qPCR and Western blotting were used to analyze mRNA and protein expression. Interleukin (IL)-13-treated human nasal epithelial cells (hNECs) was employed as the AR cell model. Cell apoptosis and viability were evaluated by TUNEL staining and MTT assay, respectively. ROS level was examined by the DCFH-DA probe. Superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px) and malondialdehyde (MDA) levels were measured by the corresponding kits. FBXW7 m6A modification level was assessed by MeRIP assay. Methods Our results showed that APS treatment reduced cell apoptosis, ROS, and MDA levels while increasing SOD, CAT, and GSH-Px levels in IL-13-treated hNECs by activating the Nrf2/HO-1 pathway. Moreover, APS alleviated IL-13-induced oxidative stress injury in hNECs by downregulating WTAP. In addition, WTAP knockdown increased FBXW7 mRNA stability by regulating FBXW7 mRNA m6A modification. It also turned out that APS alleviated IL-13-induced oxidative stress injury in hNECs through the WTAP/FBXW7 axis. Conclusions Taken together, APS inhibited WTAP-mediated FBXW7 m6A modification to alleviate IL-13-induced oxidative stress injury in hNECs.

Korean Mint (Agastache rugosa) Extract and Its Bioactive Compound Tilianin Alleviate Muscle Atrophy via the PI3K/Akt/FoxO3 Pathway in C2C12 Myotubes.

Skeletal muscle atrophy, which is characterized by diminished muscle mass, strength, and function, is caused by malnutrition, physical inactivity, aging, and diseases. Korean mint (Agastache rugosa Kuntze) possesses various biological functions, including anti-inflammatory, antioxidant, anticancer, and antiosteoporosis activities. Moreover, it contains tilianin, which is a glycosylated flavone that exerts antioxidant, anti-inflammatory, antidiabetic, and neuroprotective activities. However, no studies have analyzed the inhibitory activity of A. rugosa extract (ARE) and tilianin on muscle atrophy. Thus, the present study investigated the potential of ARE and tilianin on muscle atrophy and their underlying mechanisms of action in C2C12 myotubes treated with tumor necrosis factor-α (TNF-α). The results showed that ARE and tilianin promoted the phosphatidylinositol 3-kinase/protein kinase B pathway, thereby activating mammalian target of rapamycin (a protein anabolism-related factor) and its downstream factors. Moreover, ARE and tilianin inhibited the mRNA expression of muscle RING-finger protein-1 and atrogin-1 (protein catabolism-related factors) by blocking Forkhead box class O3 translocation. ARE and tilianin also mitigated inflammatory responses by downregulating nuclear factor-kappa B expression levels, thereby diminishing the expression levels of inflammatory cytokines, including TNF-α and interleukin-6. Additionally, ARE and tilianin enhanced the expression levels of antioxidant enzymes, including catalase, superoxide dismutase, and glutathione peroxidase. Overall, these results suggest that ARE and tilianin are potential functional ingredients for preventing or improving muscle atrophy.

Ameliorative Effect of Justicia carnea Methanol Leaf Extract against Nephrotoxicity in Streptozotocin-Induced Diabetic Wistar Rats

This study investigated the antioxidant capabilities of methanol extract from Justicia carnea leaves in streptozotocin (STZ)-induced diabetic Wistar rats, emphasizing its nephroprotective potential. Thirty-six (36) Wistar albino rats were randomized into six (6) groups (n=6/group). Group 1 served as the normal control, while groups 2-6 were induced with diabetes using 50 mg/kg of STZ intraperitoneally. Group 2 remained untreated, group 3 received 50 mg/kg body weight of Metformin, and groups 4, 5, and 6 were administered 100, 200, and 500 mg/kg body weight of the methanol Justicia carnea extract, respectively. Parameters assessed included fasting blood glucose (FBG), body weight changes, acute toxicity, and oxidative stress markers. Acute toxicity testing indicated no deaths at 5000 mg/kg of the extract. The extract significantly lowered FBG levels in STZ-induced diabetic rats (p &lt; 0.05). The control group exhibited the highest weight gain compared to the treated groups (p &lt; 0.05). Treatment with the extract notably increased catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GPx) levels, while decreasing malondialdehyde (MDA) concentrations (p &lt; 0.05) compared to diabetic controls. Overall, the methanol extract of Justicia carnea ameliorated oxidative stress in the kidneys of diabetic Wistar rats, suggesting its potential to mitigate nephrotoxicity associated with type I diabetes-induced kidney damage. These findings underscore its therapeutic promise in combating oxidative stress-related complications of diabetes.

Protective Role of Doxofylline against Cyclophosphamide-induced Testicular Toxicity in Rats

Background: Cyclophosphamide (CP) is a widely used anticancer and immunosuppressant drug. However, CP's significant toxicities and adverse effects restrict its clinical use. Doxofylline (DF) is a phosphodiesterase inhibitor that has antioxidant and anti-inflammatory properties. Objective: To determine the protective effect of doxofylline on rats exposed to a single dose of CP. Methods: We randomly assigned thirty Sprague-Dawley male rats to three groups. On the sixth day, the apparently healthy control group (AH) received normal saline; the induction group (IN) received normal saline and a single dose of CP (100 mg/kg); and the DF group received DF (50 mg/kg) and a single dose of CP (100 mg/kg). Treatment in all groups was given once daily and intraperitoneally. At the end of treatment, caudal fluid is used to determine sperm parameters. A blood sample was taken to determine the testosterone levels. We determined the levels of testicular glutathione peroxidase and malondialdehyde. The testes were harvested, allowing for histological examination. Results: Sperm parameters, testosterone and oxidative stress markers were notably declining in testicular tissue among the IN compared with AH, although these measures can be markedly improved with DF. Histopathological analysis revealed a substantial change in the testicular tissue structure in the CP group, although doxofylline co-treatment significantly attenuated and even reversed these changes. Conclusions: Doxofylline may function as a protective agent, mitigating the testicular damage caused by CP therapy in rats. The proposed process may be attributed to its phosphodiesterase inhibitory and antioxidant properties.

Enhancing cowpea wilt resistance: insights from gene coexpression network analysis with exogenous melatonin treatment

BackgroundCowpea wilt is a harmful disease caused by Fusarium oxysporum, leading to substantial losses in cowpea production. Melatonin reportedly regulates plant immunity to pathogens; however the specific regulatory mechanism underlying the protective effect of melatonin pretreated of cowpea against Fusarium oxysporum remains known. Accordingly, the study sought to evaluate changes in the physiological and biochemical indices of cowpea following melatonin treated to facilitate Fusarium oxysporum resistance and elucidate the associated molecular mechanism using a weighted gene coexpression network.ResultsTreatment with 100 µM melatonin was effective in increasing cowpea resistance to Fusarium oxysporum. Glutathione peroxidase (GSH-PX), catalase (CAT), and salicylic acid (SA) levels were significantly upregulated, and hydrogen peroxide (H2O2) levels were significantly downregulated in melatonin treated samples in roots. Weighted gene coexpression network analysis of melatonin- and Fusarium oxysporum-treated samples identified six expression modules comprising 2266 genes; the number of genes per module ranged from 9 to 895. In particular, 17 redox genes and 32 transcription factors within the blue module formed a complex interconnected expression network. KEGG analysis revealed that the associated pathways were enriched in secondary metabolism, peroxisomes, phenylalanine metabolism, flavonoids, and flavonol biosynthesis. More specifically, genes involved in lignin synthesis, catalase, superoxide dismutase, and peroxidase were upregulated. Additionally, exogenous melatonin induced activation of transcription factors, such as WRKY and MYB.ConclusionsThe study elucidated changes in the expression of genes associated with the response of cowpea to Fusarium oxysporum under melatonin treated. Specifically, multiple defence mechanisms were initiated to improve cowpea resistance to Fusarium oxysporum.

High-Intensity Interval Training Ameliorates Tramadol-Induced Nephrotoxicity and Oxidative Stress in Experimental Rats.

Tramadol (TRA) is an opioid analgesic widely prescribed for moderate-to-severe pain; however, its abuse and chronic use have been associated with kidney damage. Considering the protective role of exercise training in reducing organ damage, this study aimed to assess the influence of high-intensity interval training (HIIT) on a male rat's kidney following chronic TRA administration. In this experimental study, 30 male Wistar rats were assigned to the following groups: control (CON; animals received normal saline five days a week in the first month and three days a week in the second month), exercise (EXE; animals conducted HIIT training according to exercise protocol five days a week for two months), TRA (animals received TRA 50 mg/kg (i.p.) as described for the CON group), EXE-TRA (animals received TRA and conducted exercise protocol), and EXE-SL (animals received normal saline and conducted exercise protocol). Then, serum IL-6 and IL-10 levels, tissue malondialdehyde (MDA), total antioxidant capacity (TAC), glutathione peroxidase (GPx), superoxide dismutase (SOD), and levels of albumin, urea, and creatinine (CR), along with pathological changes in the kidney, were measured. A p-value of <0.05 was considered significant using GraphPad Prism v.9 (GraphPad Software, La Jolla, California, USA). The inflammatory cytokines IL-6 and IL-10 were significantly increased in the EXE and EXE-TRA groups compared to the TRA group. Chronic administration of TRA in the TRA group decreased antioxidant indicators TAC, GPx, and SOD in kidney tissue while increasing oxidative stress MDA compared to the CON group (p<0.05). In contrast, the EXE-TRA group showed higher levels of TAC, GPx, and SOD, while MDA decreased compared to the TRA group. Additionally, serum levels of urea and CR were increased in the TRA group compared to the CON group, whereas these levels were decreased in the EXE-TRA group compared to the TRA group. The inflammatory effect of HIIT training, due to severe hyperemia and mild inflammatory cell infiltration, was seen in all EXE groups. Pathological findings confirmed TRA-induced kidney damage through moderate hyaline cast presence and severe apoptosis in the TRA group. Other findings were in line with the above results. These findings confirm the nephrotoxicity of chronic use of TRA through biochemical and oxidative markers and pathological outcomes. In addition, the result suggests that HIIT has the potential to mitigate the detrimental effects of TRA through reversing biochemical and oxidative markers, including TRA-induced apoptosis. Consequently, considering its restorative properties, HIIT could be explored as a prospective nephroprotective approach for long-term TRA treatment.

Synergistic protective effects of 3,4-dihydroxyphenylglycol and hydroxytyrosol in male rats against induced heat stress-induced reproduction damage

Testicular heat stress disrupts spermiogenesis and damages testicular tissue. The study aims to assess 3,4-dihydroxyphenylglycol (DHPG) and hydroxytyrosol (HT) from olive oil as antioxidants to reduce heat-induced testicular damage. Seven groups of 35 male rats were used. Group I got normal saline. Group 2 had HS (43 °C for 20 min/day) and normal saline for 60 days. Groups 3–7 had HS and DHPG/HT doses (0.5 mg/kg DHPG, 1 mg/kg DHPG, 5 mg/kg HT, 0.5 mg/kg DHPG + 5 mg/kg HT, and 1 mg/kg DHPG + 5 mg/kg HT). The evaluation included tests on testicular tissue, sperm quality, oxidative status, gene activity, and fertility after 60 days. After DHPG and HT treatment, sperm motility, viability, and plasma membrane functionality, as well as levels of total antioxidant capacity (TAC), glutathione peroxidase (GPx), superoxide dismutase (SOD), and catalase (CAT), and Bcl-2 gene expression, and in vivo fertility indexes increased. Meanwhile, abnormal morphology and DNA damage decreased, along with levels of glutathione (GSH), nitric oxide (NO), and malondialdehyde (MDA), and Bax, caspase-3, and caspase-9 gene expression, compared to the HS group. The study found that DHPG and HT have a more substantial synergistic effect when used together, improving reproductive health.

Dose-dependent protective effects of Lactobacillus rhamnosus GG against stress-induced ulcer.

Stress-related diseases are on the rise and stress is one of the common factors that lead to ulcer. Stress-induced mucosal bleeding is a serious complication observed in many critically ill patients. Due to the harmful side effects of proton pump inhibitors, natural and active alternative treatment methods for peptic ulcer treatment that are safe in terms of side effects are an urgent need for human health. We aimed to investigate the dose-dependent protective effects of Lactobacillus rhamnosus GG (LGG) against stress ulcer induced by cold restraint stress in rats. This study was performed in a total of 42 rats, in control group (C), stress group (S), pantoprazole (20 mg kg-1 day-1) group (P), LGG (3 × 108 cfu mL-1 day-1) + stress group (M1), LGG (15 × 108 mL-1 day-1) + stress group (M5) and LGG (30 × 108 mL-1 day-1) + stress group (M10) (each n = 7). Ulceration areas (mm2) were determined quantitatively with ImageJ software. Glucocorticoid, catalase (CAT), superoxide dismutase (SOD) and glutathione peroxidase (GPx) levels were determined by ELISA and malondialdehyde levels were determined by spectrophotometric measurement. Histopathological examinations were performed in gastric tissue. Therapeutic dose of LGG increased CAT, SOD and GPx levels; prevented excessive activation of the hypothalamic-pituitary-adrenal axis; reduced ulceration and bleeding in the gastric mucosal layer; and provided stabilization of mast cells. We can suggest that LGG may be beneficial for reducing the negative effects of stress on the body, for protecting against ulcer disease and for reducing or preventing the risk of stress-induced gastrointestinal bleeding in patients staying in intensive care units. © 2024 The Author(s). Journal of The Science of Food and Agriculture published by John Wiley & Sons Ltd on behalf of Society of Chemical Industry.

Evaluation of enzymatic antioxidant activity and reproductive hormones near and after lambing in pregnant ewes

The current study examined the levels of antioxidants superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px), glutathione (GSH), and Malondialdehyde (MDA) and repro ductive hormones (progesterone, estrogen, and cortisol) in pregnant local breed ewes and after lambing in the Basrah governorate. Twenty ewes were used in this study from several fields in the Basrah gov ernorate. Blood sample collection was done in three different periods, pre-lambing, immediately after lambing, and two weeks after lambing. The result showed a significant decrease (p&lt;0.05) in SOD, CAT, and GSH-px activity before and during lambing compared to after lambing. The results also con firmed a significant increase (p&lt;0.05) in the level of GSH pre and during lambing compared to after lambing. While evaluating, the level of MDA revealed a significant increase (p&lt;0.05) in its level dur ing lambing compared to two weeks after lambing. Hormonal analysis showed a significant increase (p&lt;0.05) in the levels of cortisol and estradiol pre and during lambing compared to after lambing, with a significant decrease (p&lt;0.05) in the levels of progesterone after lambing compared to before lambing. This study concluded that during lambing, ewes were under stress factors, and an internal mechanism represented by enzymatic antioxidants like SOD, CAT, and GSH-Px acted actively during this period to neutralize the side effects of stress.

Attenuation of Cadmium Toxicity by Methanol Extracts of Rauvolfia vomitoria and Aframomum melegueta leaves

Highlights:1. This study provides insight into the detrimental effect of cadmium exposure on mammalian cells using a murine model.2. The co-administration of Rauvolfia vomitoria and Aframomum melegueta leaf extracts is more effective in ameliorating cadmium-induced toxicity than a single administration of each plant extract.3. The co-administration of Rauvolfia vomitoria and Aframomum melegueta plant extracts can upregulate the expression of IL-10 and reverse the derangements in the TNF-α, IL-6, SOD, and GPX levels. Abstract Cadmium has long been known to be an environmental pollutant that can harm human health, with toxicity majorly affecting the kidneys and liver. This study aimed to investigate the mitigating potential of methanol extracts of Rauvolfia vomitoria and Aframomum melegueta leaves in cadmium-induced liver toxicity. Twenty-five male adult Wistar rats, averagely weighing 200 g, were randomly allocated into five groups, each comprising five rats. Group 1 was unexposed to any substances and only received distilled water. Group 2 was given cadmium at a standard dose of 12 mg/kg bw. Groups 3, 4, and 5 received 12 mg/kg bw of cadmium, and each group was treated with 200 mg/kg bw of Rauvolfia vomitoria leaf extract, Aframomum melegueta leaf extract, and a combination of both extracts, respectively. After 28 days, the animals were euthanized to obtain their livers, which were then excised and processed for histopathological, mRNA expression, and biochemical analyses. A one-way analysis of variance (ANOVA) was used to analyze the data, and Duncan multiple tests were employed to compare the categorical variables (p&lt;0.05). The results revealed elevated levels of interleukin 10 (IL-10) in the rats treated with Rauvolfia vomitoria and Aframomum melegueta extracts when compared to Group 2. On the other hand, the treatment groups exhibited a significant decrease in tumor necrosis factor alpha (TNF-α) and interleukin 6 (IL-6) levels, along with significantly elevated levels of superoxide dismutase (SOD) and glutathione peroxidase (GPx). Group 5 showed a normal liver histoarchitecture similar to Group 1, reversing the histopathological abnormalities shown in Group 2. In conclusion, the co-administrative treatment using Rauvolfia vomitoria and Aframomum melegueta extracts reversed the cadmium-induced toxicity better than using each plant extract individually. This further suggests that Rauvolfia vomitoria and Aframomum melegueta leaf methanol extracts may ameliorate the effects of cadmium-induced toxicity, including reducing oxidative stress and fortifying the anti-oxidant system.