Background: Nitrate (NO3) is the most common chemical contaminant in the world’s ground water aquifer. Oxidative stress has been proposed as a possible mechanism involved in NO3 toxicity on non-target organism. Objectives: The current study aimed to elucidate the potential protective effect of Telfairia occidentalis (pumpkin seed oil, PSO) against hepatotoxicity induced by sodium nitrate. Methods: Wistar rats were exposed either to NaNO3 (200 mg/kg bw) in drinking water in drinking water, or to 4ml PSO/kg bw by gavage or to their combination. Oxidative stress parameters, biochemical biomarkers and liver histopathological examination were determined. Results: Our data showed that the exposure of rats to NaNO3 caused significant changes of some haematological parameters compared to the control. In addition, there was a significant elevation of the levels of biochemical markers as that of aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase and lactate dehydrogenase when compared with the control. Furthermore, exposure of rats to NaNO3 induced liver oxidative stress as indicated by the increase of malondialdehyde, pro- gressive oxidation of protein products and protein carbonyl levels. In addition, a reduction in anti-oxidant status (catalase, glutathione peroxidase, glutathione-S-transferase and superoxide dismutase, reduced glutathione and vitamin C) was observed. Conclusion: Co-administration of PSO to the NaNO3 restored most parameters cited above to near-normal values. Therefore, the present investigation revealed the ability of PSO to attenuate NaNO3-induced oxidative damage. Keywords: Sodium nitrate; Telfairia occidentalis; pumpkin seed oil; hepatotoxicity; oxidative stress; protection; anti-oxidant status, rat.

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The present study focused on the protective efficacy of Allium sativum oil (ASO) against tebuconazol (TEB)-induced oxidative stress in the liver of adult rats. Thirty-two rats were randomly divided into four groups of eight each: group I served as control rats, group II was treated with TEB (100 mg/kg bw), group III received ASO (5ml/kg bw). The animals of group IV were treated with TEB and ASO, during 4 weeks. The obtained results showed that TEB induced a significant change of some hematological parameters, including red blood cells (RBC), haemoglobin content (Hb), haematocrit (Ht), white blood cells (WBC) and platelet (Plt) compared to the control group. Moreover, while the total cholesterol levels and the activities of aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), lactate dehydrogenase (LDH) and γ-Glutamyltranspeptidase (γGT) significantly increased due to TEB administration, the concentrations of plasma total protein, albumin and triglyceride considerably decreased. Furthermore, the exposure to TEB significantly increased the malondialdehyde (MDA), protein carbonyl (PCO) and advanced oxidation protein products (AOPP) levels and decreased glutathione peroxidase (GPx), superoxide dismutase (SOD), catalase (CAT) and glutathione-S-transferase (GST) activities in the hepatic tissues. The results were confirmed by the histological impairments. Besides, the co-administration of ASO improved the status of all studied parameters. Therefore, our investigation revealed that ASO had protective effects against TEB-induced liver injury, which could be attributed to its phenolic compounds.