N-acetylcysteine ​​protects against acyclovir-induced nephrotoxicity

N-acetylcysteine ​​protects against acyclovir-induced nephrotoxicity

Background and goals

Oxidative stress may be a key process in the nephrotoxicity induced in acyclovir (ACV). N-Acetylcysteine ​​(NAC) is a water-soluble antioxidant with anti-inflammatory activity. This study aimed to evaluate the protective effect of NAC on ACV-induced nephrotoxicity in adult Wistar rats.

Methods

Forty adult male Wistar® rats (200-220 g) were used. The rats were randomly divided into eight groups (n = 5/group) and treated intraperitoneally for seven days as follows:Group 1 (control) was administered water (0.2 ml), while groups 2-4 were administered NAC (25, 50 and 100 mg/kg). Group 5 was administered ACV (150 mg/kg), while groups 6–8 were supplemented with NAC (25, 50, and 100 mg/kg) before treatment with ACV (150 mg/kg). On day 8, rats were weighed and euthanized, and blood samples were collected for assessment of biochemical markers. Kidneys were weighed and subjected to oxidative stress markers and histological assessments.

Results

ACV had no significant (P> 0.05) Effects on the body and kidney weights of rats compared to the control. ACV produced significantly (P<0.001) Increases in renal malondialdehyde, serum urea, creatinine and uric acid in rats different from control. There were significant (P<0.001) Decrease in renal glutathione, superoxide dismutase, peroxidase and catalase as well as serum chloride, potassium, bicarbonate and sodium levels in ACV-treated rats compared to control. ACV led to expansion of Bowman's space and tubular necrosis in the kidneys of rats. Nevertheless, NAC supplementation abolished ACV-induced nephrotoxicity in a dose-dependent manner. Renal histology was restored by NAC supplementation.

Conclusions

NAC protected against ACV-induced nephrotoxicity. This finding indicates that NAC may have therapeutic potential for nephrotoxicity through ACV.

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