Protective Role of Vitamin E Against Cadmium-Induced Renal Oxidative Stress in Adult Male Wistar Rats.

Cadmium (Cd), a widely distributed heavy metal, is extremely toxic to the kidney. The toxicity of cadmium is closely linked to its pro-oxidant properties, which increase oxidative stress, thereby damaging cells and causing various health issues.
Vitamin E (VE) is a group of eight compounds that share a similar molecular structure. These include four tocopherols and four tocotrienols, with tocopherols being the most widely recognized for their antioxidant properties that help protect cell membranes. This protection of cells is crucial for maintaining overall health, particularly in preventing oxidative stress-related conditions.
This study investigates the protective role of vitamin E against the effects of cadmium exposure on kidney function, focusing on key antioxidants: glutathione (GSH), oxidized glutathione (GSSH), glutathione-S-transferase (GST), and glutathione peroxidase (GPx). 
A total of 30 adult male Wistar rats were randomly divided into six groups: Group 1 (control) received distilled water (1 ml), group 2 was received CdCl₂ (30 mg/kg), group 3 received CdCl₂ (30 mg/kg) and DSaq (200 mg/kg), group 4 received CdCl₂ (30 mg/kg) and DSaq (100 mg/kg), group 5 was treated with DSaq alone (200 mg/kg), and group 6 received CdCl₂ (30 mg/kg) along with Vitamin E (standard dose). Datura stramonium was administered orally for 28 days, the Cadmium Intraperitoneally only on the first day and Vitamin E Intramuscularly on days 1, 7, 14 & 21.
The results indicated that cadmium exposure significantly affected GSH, GSSH levels and GST and GPx activities, indicative of oxidative damage. However, vitamin E supplementation mitigated these effects, enhancing the antioxidant defense system and reducing oxidative stress markers.
The findings suggest that vitamin E offers protective benefits against cadmium-induced renal damage by modulating antioxidant enzymes and GSH metabolism.