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Environmental pollution remains a major global health concern, particularly when it comes to heavy metals, which are associated with various health hazards. Among the prevalent heavy metals in the environment is cadmium (Cd). As a result, the current study aimed to investigate the nephroprotective potential of olive leaves extract (OLE) against Cd-induced chronic renal injury. Forty-eight albino rats were divided into four equal groups. Rats in the control group were received distilled water orally, while those in the OLE group were orally administered OLE 200 (mg/kg b.wt.) daily. The cadmium-intoxicated group rats were orally gavage 5 mg Cd/kg b.wt. twice a week and the OLE+Cd group received the same doses of both OLE and CdCl2. After 4 and 8 weeks of the experiment, blood and kidney samples were collected for analysis of kidney function test and histopathological examination. Oral administration of cadmium chloride (CdCl2) for 4 and 8 weeks resulted in nephrotoxicity, evidenced by a significant increase (P<0.05) in urea, uric acid, and creatinine levels. These biochemical changes were accompanied by distinct histopathological alterations, including renal hemorrhage, edema and vasculitis with severe glomerular and tubular necrosis as well as periglomerular fibrosis and marked interstitial fibrosis. Treatment with OLE exhibited a remarkable reduction in these histopathological changes and restored the serum parameters toward normal levels. In conclusion, OLE has a time-dependent mitigating effect against Cd-induced nephrotoxicity by reducing inflammation, glomerulotubular injury, and renal fibrosis, indicating that it is a potential natural product in counteracting chronic nephrotoxicity. [ABSTRACT FROM AUTHOR]

Cadmium (Cd) is a well-known industrial and environmental pollutant having hazardous and poisonous properties in various forms of kidney impairment. Consequently, this study aimed to evaluate the nephroprotective effect of palm dates extract (PDE) and olive leaves extract (OLE) against cadmium chloride (CdCl2)-induced nephrotoxicity. A total of 36 adult male albino rats were divided into six equal groups. Group 1: control group injected with physiological saline, group 2: oral gavage with PDE, group 3: orally administrated with OLE, group 4: injected daily with CdCl2 (3 mg/kg, i.p.). Groups 5 and 6: were orally treated with either PDE or OLE, respectively one hour prior to ip administration of CdCl2. After one-week samples were collected from all groups for serum biochemical analysis of kidney function as well as investigation of malondialdehyde (MDA), catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GPx). Kidney tissue specimens were obtained for histopathological examination. CdCl2 exposure caused a significant elevation (P<0.05) in serum creatinine, urea, uric acid and MDA levels with marked reduction in CAT, SOD and GPx indicating renal damage. CdCl2 induced severe congestion and vasculitis with marked perivascular edema, inflammation, hemorrhage, glomerular shrinkage, massive degeneration, necrosis and apoptosis in the renal tubular epithelium. PDE and OLE treatment resulted in significant improvement in kidney function and oxidative markers with a marked reduction of MDA level. Histopathological changes were also ameliorated. In conclusion, PDE or OLE treatment significantly reduced the deleterious effects of acute CdCl2 renal damage by reducing oxidative stress as a protective mechanism. [ABSTRACT FROM AUTHOR]