Antioxidant enzymes

Arsenic exposure remains a major environmental health concern due to its ability to generate oxidative stress and induce tissue injury, particularly in the liver. This study investigated the protective potential of rutin against sodium arsenite-induced hepatic oxidative damage in Wistar rats. The experiment involved the administration of sodium arsenite to induce oxidative stress,
while rutin was concurrently given at different doses to evaluate its antioxidant and hepatoprotective effects. Following treatment, liver antioxidant status was assessed through the measurement of key biochemical parameters including reduced glutathione (GSH), superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx). Histopathological examination of liver tissues was also carried out to determine structural alterations associated with arsenite toxicity and the possible protective influence of rutin. The results indicated that exposure to sodium arsenite caused a pronounced decline in endogenous antioxidant defenses, reflected by reduced levels of GSH and decreased activities of SOD, CAT, and GPx. These biochemical disruptions were accompanied by noticeable histological abnormalities in hepatic tissue, suggesting oxidative damage and cellular
degeneration. However, rats that received rutin alongside sodium arsenite demonstrated marked improvement in antioxidant enzyme activities and glutathione levels compared with animals treated with arsenite alone. The degree of improvement was more pronounced at higher rutin doses, indicating a dose-dependent protective effect. The findings suggest that rutin exerts significant antioxidant activity capable of counteracting arsenite-induced oxidative stress in the liver. This protective action may be attributed to its ability to scavenge reactive oxygen species and enhance endogenous antioxidant defense mechanisms.
onsequently, rutin may serve as a promising natural compound for reducing oxidative damage associated with heavy metal toxicity. In conclusion, the study demonstrates that rutin effectively mitigates sodium arsenate-induced hepatic oxidative injury in Wistar rats by restoring antioxidant balance and improving liver tissue integrity.

Nickel chloride (NiCl2) is a widespread environmental contaminant that causes neurotoxicity, with the cerebellum showing particular vulnerability due to its central role in motor coordination and high metabolic demands. Memantine, a non-competitive
N-methyl-D-aspartate (NMDA) receptor antagonist. It is hypothesized that its neuroprotective properties could be beneficial in the mitigation of cerebellar damage caused by nickel chloride. This study was aimed at investigating the effects of memantine on the nickel chloride induced cerebellar toxicity in wistar rats. Forty-eight rats were divided into eight groups: Control, nickel chloride only, high dose of memantine + nickel chloride, low dose of memantine + nickel chloride, high dose of memantine, low dose of memantine. The treatment protocol ran for 28 days. A served as control and received 1ml of distilled water daily to compensate for stress of administration, whereas, rats in group B received 2.5mg/kg of NiCl₂, rats in group C received 10mg/kg Og memantine(low dose) and 2.5mg/kg of NiCl₂, rats in group D received 20mg/kg of memantine (high dose) and 2.5mg/kg of NiCl₂, rats in group E received 10mg/kg of memantine (low dose) and rats in group F received 20mg/kg of memantine (high dose). Administration of memantine was done orally using an orogastric tube while the administration of nickel chloride was done via intraperitoneal injection. It lasted for 28days. The body weight of the rats were recorded daily. At the end of the experimental period, the rats were sacrificed by cervical dislocation and the organ( cerebrum) weight was recorded. The parameters accessed include cerebral antioxidant enzymes (SOD, CAT, GPx and GSH), MDA concentration and the histology of the cerebrum using
Hematoxylin and Eosin staining technique. Results obtained showed no significant change (p>0.05) in the initial body weight and final body weight. A significant decrease (p<0.05) was observed in the weight change of rats in group B when compared to control, however, a significant increase (p<0.05) was observed in the weight of groups C and D when compared to group B. No significant change (p>0.05) was observed in the cerebellar and relative cerebellar weight of rats across experimental groups. A significant decrease (p<0.05) was observed in cerebellar SOD, CAT, GPx and GSH activity of rats in group B (2.5 mg/kg bw. NiCl2) when compared to the control. A significant increase (p>0.05) in cerebellar MDA concentrations was observed in the weights of rates in group B (2.5 mg/kg bw. NiCl2 ) when compared with group A. Severe histological alterations in the cerebellum of nickel-chloride exposed rats were observed. However, pre-treatment with memantine mitigated the adverse effects induced by NiCl2. In conclusion, findings from this study shows that memantine exerted antioxidant properties as well as mitigating the histological alterations in the cerebellum.