Nephroprotective Potential Of Glucosamine Against Cadmium Chloride-Induced Kidney Injury In Rats

Cadmium contributes to nephrotoxicity in humans and animals by inducing oxidative stress. The dataset demonstrates the in vivo renal histology and biochemical activity of Glucosamine (Chitosamine) in cadmium-induced nephrotoxic rat model. A total of 42 female albino Wistar rats weighing between 180 to 220 g were categorized into seven groups (n=6). Except for the first group (control), all of the groups received CdCl2 5mg/kg body weight per oral (p.o). Second-group is the negative control group (toxic, CdCl2 treated), the third and fourth received EDTA 495mg/kg, and Vitamins 50mg/kg (p.o) respectively. Glucosamine 0.2g/kg (p.o) was given to the fifth and sixth groups, whereas Vitamins 50mg/kg (p.o) were given to the sixth and seventh groups, respectively. Seventh group additionally received EDTA 495mg/kg (p.o). Kidney function parameters were estimated in serum and oxidative damage parameters and histopathology were estimated in kidney tissues. Cadmium chloride raised, blood urea nitrogen (BUN), creatinine (Cr), uric acid, urea and tissue malondialdehyde (MDA) levels while decreasing tissue superoxide dismutase (SOD), glutathione (GSH), and catalase (CAT) levels. Glucosamine administration significantly reduced lipid peroxidation, enhanced glutathione and antioxidant enzyme activities, and considerably lowered BUN and creatinine levels. Data were supported by histological examination indicated improved changes in kidney, indicating protective potential of Glucosamine in cadmium chloride-induced nephrotoxicity.