19 research outputs found
Diclofenac – induced hepatotoxicity: Low dose of omega-3 fatty acids have more protective effects
No full textThe global embrace of the Western dietary style has necessitated the need for supplementation with omega-3 fatty acids (N-3) to redress the imbalance in omega-6/omega-3 fatty acids ratio. Therefore, the study investigated the effects of pre-treatment with N-3 in adult male Wistar rats exposed to diclofenac sodium (DF). Twenty adult male Wistar rats were used for this study. They were divided into 4 groups of 5 rats each, which included: Group 1 - Normal control; Group 2 - DF control; Group 3 - Low N-3 + DF; and, Group 4 - High N-3 + DF. The rats in group 2 were administered DF (10 mg/kg b.w./day, im) during the last 7 days of the experiment, while the rats in groups 3 and 4 were pre-treated with N-3 at 100 and 300 mg/kg b.w./day, po respectively for 21 days, afterwards, they received DF at 10 mg/kg b.w./day (im) for 7 days. The result showed that DF significantly increased malondialdehyde, lactate dehydrogenase, and pro-inflammatory markers (total white blood cell count, uric acid, platelet/lymphocyte and neutrophil/lymphocyte ratios). Moreover, DF significantly elevated the activities of alanine aminotransferase, aspartate aminotransferase, and alkaline phosphatase, but, significant reduced the total antioxidant capacity and the activities of superoxide dismutase, catalase, and glutathione peroxidase. The histological results were parallel to the biochemical and haematological findings. Pre-treatment with N-3 significantly prevented the manifestation of the abnormalities brought about by DF. Although there were indications of the dose-dependent effects of N-3, the low dose was found to be more effective. In conclusion, the pre-administration of N-3, preferably at a low dose, could reduce hepatotoxicity that could result from subsequent exposure to DF. Keywords: Omega-3 fatty acids, Hepatoprotective, Diclofenac, Inflammation, Oxidative stres
Calcitonin and Omega–3 Fatty Acids Exhibit Antagonistic and Non-Additive Effects in Experimental Diabetes
No full textSynergistic and non-synergistic effects of salmon calcitonin and omega - 3 fatty acids on antioxidant, anti-inflammatory, and haematological indices in diabetic rats
No full textOmega-3 fatty acid ameliorates bisphenol F-induced testicular toxicity by modulating Nrf2/NFkB pathway and apoptotic signaling
No full textIntroductionBisphenol F (BPF) has been shown to disrupt testicular functions via perturbation of testicular redox balance, while omega-3 fatty acid (O3FA) has been established to exert antioxidant and anti-inflammatory activities. Therefore, this study focused on the role and associated molecular mechanism of O3FA in BPF-induced testicular dysfunction in male Wistar rats.MethodsTwenty-four (24) rats were randomly grouped after two weeks of acclimatization into four (4) groups (n=6/group); the vehicle-treated control group, BPF treated group received 30 mg/kg of BPF, and the intervention groups received 30 mg/kg BPF + 100 mg/kg O3FA (BPF+O3FA-L) and 30 mg/kg BPF + 300 mg/kg of O3FA (BPF+O3FA-H). All treatment lasted for 28 days.ResultsLow and high doses of O3FA ameliorated BPF-impaired sperm quality, and induced hormonal imbalance, accompanied by a distortion in testicular histology and elevated testicular injury markers. Furthermore, co-administration of BPF with both doses of O3FA blunted BPF-induced redox imbalance, inflammatory response, and apoptosis.DiscussionsIn conclusion, our present findings show that O3FA improves testicular functions in BPF-treated rats by improving sperm quality and reproductive hormones via the maintenance of testicular redox balance
Image_1_Omega-3 fatty acid ameliorates bisphenol F-induced testicular toxicity by modulating Nrf2/NFkB pathway and apoptotic signaling.jpeg
No full textIntroductionBisphenol F (BPF) has been shown to disrupt testicular functions via perturbation of testicular redox balance, while omega-3 fatty acid (O3FA) has been established to exert antioxidant and anti-inflammatory activities. Therefore, this study focused on the role and associated molecular mechanism of O3FA in BPF-induced testicular dysfunction in male Wistar rats.MethodsTwenty-four (24) rats were randomly grouped after two weeks of acclimatization into four (4) groups (n=6/group); the vehicle-treated control group, BPF treated group received 30 mg/kg of BPF, and the intervention groups received 30 mg/kg BPF + 100 mg/kg O3FA (BPF+O3FA-L) and 30 mg/kg BPF + 300 mg/kg of O3FA (BPF+O3FA-H). All treatment lasted for 28 days.ResultsLow and high doses of O3FA ameliorated BPF-impaired sperm quality, and induced hormonal imbalance, accompanied by a distortion in testicular histology and elevated testicular injury markers. Furthermore, co-administration of BPF with both doses of O3FA blunted BPF-induced redox imbalance, inflammatory response, and apoptosis.DiscussionsIn conclusion, our present findings show that O3FA improves testicular functions in BPF-treated rats by improving sperm quality and reproductive hormones via the maintenance of testicular redox balance.</p
Combined but not single administration of vitamin C and<scp>l</scp>-carnitine ameliorates cisplatin-induced gastric mucosa damage in male rats
No full textAlthough cisplatin is a potent anticancer drug, it instigates oxidative and pro-inflammatory reactions that pose significant and distressing clinical symptoms. Therefore, this study investigated the effects of vitamin C and (or) l-carnitine on cisplatin-induced gastric mucosa damage in rat. The rats were allocated into 6 groups (n = 5). The control group received distilled water, while the treatment groups received cisplatin alone (CIP), or cisplatin with vitamin C, l-carnitine, or their combination. Cisplatin caused disruption of the gastric mucosa histoarchitecture and altered the mucus barrier function. Moreover, the stomach tissue of the CIP-treated group showed increased levels of oxidative stress markers (malondialdehyde and H2O2) and decreased activities of antioxidant (superoxide dismutase, glutathione peroxidase, catalase, glutathione S-transferase) and non-antioxidant (reduced glutathione) enzymes. These deleterious events were accompanied with significant increases in pro-inflammatory cytokines and inflammatory infiltration markers, myeloperoxidase and inducible nitric oxide synthase. However, the administration of both vitamin C and l-carnitine, and not either of the two showed additive effects in attenuating the adverse effects of cisplatin. The histological results agreed with the biochemical assays. The study concluded that the combined administration of vitamin C and l-carnitine, but not the single therapy, could prevent the adverse effects of cisplatin on gastric tissue.</jats:p
Melatonin prevents and ameliorates lead-induced gonadotoxicity through antioxidative and hormonal mechanisms
No full text We investigated the effects of melatonin on sperm parameters and some biochemical markers in lead-exposed male Wistar rats. Lead (50 mg/kg bw/day) and/or melatonin (4 mg/kg or 10 mg/kg bw/day) was administered for 4 weeks, while 2-week lead exposure was preceded by or followed by 2-week treatment with both doses of melatonin in other groups. Lead reduced glutathione, catalase, adjusted testes weight, semen parameters but did not change malondialdehyde (MDA), superoxide dismutase (SOD), glutathione peroxidase, and total antioxidant capacity. Though independent of prolactin, lead-induced gonadotoxicity was both centrally and peripherally mediated, as it reduced gonadotropin-releasing hormone and testosterone levels, while gonadotropin levels did not change significantly probably due to negative feedback by elevated estradiol. However, pre-, simultaneous, or posttreatment of lead-exposed rats with melatonin reduced MDA, SOD, and estradiol but dose-dependently increased other parameters. Conclusively, lead causes male gonadotoxicity through oxidative stress and endocrine mechanisms, and these could be dose-dependently prevented and ameliorated by melatonin. </jats:p
Dietary Supplementation with D-Ribose-L-Cysteine Prevents Hepatic Stress and Pro-Inflammatory Responses in Male Wistar Rats Fed a High-Fructose High-Fat Diet
No full textDiets rich in fats and fructose are associated with the pathogenesis of oxidative stress-induced non-alcoholic fatty liver disease. Therefore, we investigated the effect of D-ribose-L-cysteine (DRLC) in high-fructose high-fat (HFHF) diet-fed rats. Twenty rats (n = 5), divided into four groups, were simultaneously exposed to HFHF and/or DRLC (250 mg/kg) orally during the 8 weeks of the study. Results showed that HFHF precipitated pro-inflammation and selective disruption of the oxidative stress markers. There were significant decreases in the level of antioxidants such as superoxide dismutase (SOD), glutathione peroxidase (GPX), total antioxidant capacity (TAC), hepatic SOD and GPX. Significant increases in serum levels of uric acid (UA), tumour necrosis factor-alpha (TNF-α), C-reactive protein (CRP) and hepatic Xanthine oxidase (XO) were observed in the HFHF compared to the control. In the HFHF + DRLC group, oxidative stress was mitigated due to differences in serum levels of SOD, GPX, TAC, TNF-α, liver SOD, and XO relative to control. The administration of DRLC alone caused significant reductions in malondialdehyde, UA and CRP and a significant increase in SOD compared to the control. DRLC prevents hepatic and systemic oxidative stress and pro-inflammatory events in HFHF diet-fed rats
Bacterial Zoonotic Diseases and Male Reproduction
No full textBacterial zoonotic diseases hold significant public health importance due to their substantial contribution to human morbidity and mortality. These infections have been implicated in reducing the fertility rate among couples of reproductive age. Despite the increasing prevalence of infertility and sub-fertility in men, there has been limited investigation into the possible effects of bacterial zoonotic infections on the male reproductive system. The purpose of this review is to describe common bacterial zoonotic diseases and their effects on human reproduction in order to unveil the hidden roles these infections could play in male factor infertility. While there is a dearth of information on this subject from human studies, available evidence from experimental animals suggests that bacterial zoonotic diseases impair male reproductive functions and structures primarily through the activation of the inflammatory response and distortion of the antioxidant system, resulting in the generation of oxidative species. In light of the limited research on bacterial zoonotic diseases and their role in male reproduction, efforts must be directed towards the subject to unravel the underlying pathological mechanisms and reduce the incidence among the human populace, either through preventive or curative measures
