Biochemical and Histological Assessment of Kidney Function in Diclofenac-Induced Toxicity Treated With Vitamin C

Non-steroidal anti-inflammatory drugs (NSAIDs) are frequently used as analgesics. Diclofenac (DIC) is one of the NSAIDs with analgesic, anti-inflammatory and anti-pyretic properties. Previous studies reported that DIC administration results in the production of reactive oxygen species (ROS) leading to DIC oxidative stress. In addition, it has been reported that is linked with nephrotoxicity, hepatoxicity reproductive toxicity and neurotoxicity. Acute kidney injury (AKI) is generally defined as a drop in kidney function resulting in piling up of waste products in the bloodstream. There are many causes of AKI includes: nephrotoxins, oxytetracycline, aminoglycosides and nonsteroidal anti-inflammatory drugs (NSAIDs). Diclofenac is often prescribed in both human and veterinary practices as an anti-inflammatory. Vitamin C (also known as ascorbic acid and ascorbate) is a water-soluble vitamin found in citrus and other fruits, berries and vegetables. It is also a generic prescription medication and in some countries is sold as a non-prescription dietary supplement. As a therapy, it is used to prevent and treat scurvy, a disease caused by vitamin C deficiency. 25 Adult male Wistar rats were selected for the study and were ivided into four groups (n=5) Group A served as the control and received only distilled water (P.O); group B rats were administered vitamin C only (i.p), group C with 100 mg/kg (i.p) of diclofenac only, group D with 100 mg/kg (i.p) body weight (BW) of diclofenac + vitamin. Results showed, amelioration of diclofenac-induced histopathological damages by vitamin C. In the control group, no pathological abnormalities were seen and there were normal distribution of cell with well defined nuclei, however, in contrast, marked morphological changes will be visualized in groups exposed to Diclofenac and these were improved on treatment with vitamin C. Also, vitamin C attenuated diclofenac-elicited reduction of enzymatic antioxidants and elevation of malondiadehyde activities. The rate of lipid peroxidation by melondiadehyde, was subsequently reduced with vitamins supplements. Conclusively, the administration of vitamin C improved the biochemical parameters (markers of oxidative stress) as well as the effects of diclofenac on histopathogical evaluations which was also attenuated and mitigated by Vitamin C. The therapeutic properties of vitamin C are multifaceted, therefore, it can be explored in further studies for treatment of renal diseases.