A renoprotective role of chitosan against lithium-induced renal toxicity in rats

Abstract

Background: Lithium (Li) is considered as the first therapeutic line for treatment of bipolar affective disorders and manic-depressive illness. Renal toxicity can be categorized as the most common undesirable side effect of Li therapy. Therefore, the present study aimed to reveal efficiency of chitosan (CS) as a natural chelator against renal toxicity induced as a result of Li injection. During current experiment, the renal functions (urea, creatinine, blood urea nitrogen (BUN), uric acid and total protein) were determined in serum samples. The urinary excretion of N-acetyl-β-Dglucosaminidase (NAG) was assayed through measuring its level in urine samples. Moreover, markers of the oxidative stress (superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), reduced glutathione (GSH) and lipid peroxidation product (LPO)) were assessed in renal tissues. In addition, histopathological and ultrastructural examinations were carried out in that tissue. Results: It was found that Li injection caused significant (P < 0.05) elevation in serum urea, creatinin and BUN levels associated with decline in uric acid and T. protein. Moreover, Li increased the urinary excretion of NAG significantly (P < 0.05). Administration of CS orally restored levels of these measurements to normalcy in CS pre-treated group through lowering urea, creatinin, BNU levels and urinary excretion of NAG with enhancing uric acid and T. protein levels. On the other hand, it was found that Li caused significant (P < 0.05) elevation in the LPO level associated with decline in activity of the antioxidant system in the renal tissues. Likewise, it caused severe alterations in the renal levels at histopathological and ultrastructural levels. The treatment with CS reduced the renal LPO associated with stimulating the antioxidant system through increasing levels of SOD, CAT, GPx and GSH in addition to its beneficial role against the histopathological abnormalities. Conclusions: The CS exhibited promising role in the protection against the oxidative stress and renal toxicity induced as a result of Li injection.

Ehrlich ascites carcinoma provokes renal toxicity and DNA injury in mice: Therapeutic impact of chitosan and maitake nanoparticles

“…Chitosan and maitake nanostructures have great capability to sharpen the antifree radical system through the elevation of GSH and catalase levels. These results complied with Aboulthana and Ibrahim, 41 who exemplified the reno-protective influence of chitosan towards renal impairment induced by lithium. Further, agreed with literature, 42 Santos et al previously indicated that the evacuation of oxidative free radicals, particularly the hydroxyl radicals driven to eminent advancement in renal function of cisplatin-induced renal toxicity rats.…”

Investigation of the Effects of Silymarin and Vitamin C on Kidney Damage and Aquaporin-2 Downregulation in Lithium-Induced Nephrogenic Diabetes Insipidus in Rats

“…Shaterpour et al [55] reported that focal moderate lymphocytic infiltrations were observed in the interstitial area in the renal tissue of the group administered LIT. Again, Aboulthanae and Ibrahim [56] detected tubular degeneration in the kidney cortex and vacuolization in the endothelial cells lining the glomerular clusters in the LIT-treated group. In the present study, it was observed that the normal structure was preserved in the renal cortex and medulla of the CNT, SIL, Vit C, and SIL+Vit C groups, and no histopathological changes were observed.…”

To Evaluate The Pernicious Histological Changes Of the Thickness Of Purkinje Cell Layer After Lithium Carbonate Ingestion

“…After three weeks animals were sacrificed, brain was removed and the cerebellum was separated from the rest of the brain and fixed in formaldehyde 8 for 24 hours.…”