Context:Nitraria retusa (Forssk.) Asch. (Nitrariaceae) is a medicinal plant which produces edible fruits whose antioxidant activity has been demonstrated.Objective: The current study elucidates the potential protective effect of N. retusa fruit aqueous extract against nephrotoxicity induced by penconazole, a triazole fungicide, in the kidney of adult rats.Materials and methods: Adult Wistar rats were exposed either to penconazole (67 mg/kg body weight), or to N. retusa extract (300 mg/kg body weight) or to their combination. Penconazole was administered by intra-peritoneal injection every 2 days from day 7 until day 15, the sacrifice day, while N. retusa extract was administered daily by gavage during 15 days. Oxidative stress parameters, kidney biomarkers and histopathological examination were determined.Results:Nitraria retusa extract administration to penconazole treated rats decreased kidney levels of malondialdehyde (−10%), hydrogen peroxide (−12%), protein carbonyls (PCOs, −11%) and advanced oxidation protein products (AOPP, −16%); antioxidant enzyme activities: catalase (−13%), superoxide dismutase (−8%) and glutathione peroxidase (GPx, −14%), and the levels of non-enzymatic antioxidants: non-protein thiols (−9%), glutathione (−7%) and metallothionein (−12%). Furthermore, this plant extract prevented kidney biomarker changes by reducing plasma levels of creatinine, urea, uric acid and LDH and increasing those of ALP and GGT. Histopathological alterations induced by penconazole (glomeruli fragmentation, Bowman’s space enlargement, tubular epithelial cells necrosis and infiltration of inflammatory leucocytes) were attenuated following N. retusa administration.Discussion and conclusion: Our results indicated that N. retusa fruit extract had protective effects against penconazole-induced kidney injury, which could be attributed to its phenolic compounds.
Data on the individual nephrotoxic effects of imidacloprid (IMI) and gibberellic acid (GA) are scarce. Moreover, there is a lack of information about their combined effects on the renal tissue. Our study investigated the effects of IMI and GA separately or together on rats kidney. IMI (64 mg/kg bw) was given for 3 weeks by gavage either individually or in combination with GA (200 mg/L) via drinking water. IMI associated or no with GA increased the levels of kidney malondialdehyde, advanced oxidation protein products, protein carbonyls and metallothionein, plasma creatinine, urea, blood urea nitrogen and lactate dehydrogenase activity. A decline of kidney uric acid level and antioxidant status was also observed. All these changes were supported by histopathological observations. Our results highlighted the role of IMI and/or GA-induced nephrotoxicity. Co-exposure to IMI and GA exhibited synergism in biochemical kidney variables and histopathology and antagonism in physical and morphological parameters.
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