Urinary exosomes are nano-sized vesicles secreted into urine from all types of renal epithelial cells and are known to contain possible biomarker proteins for renal diseases. Gentamicin has been reported to decrease the level of renal aquaporin (AQP)2, which is known to be mainly expressed in renal collecting ducts and excreted into the urine via exosomes. In the present study, we investigated whether urinary exosomal AQP2 could serve as a potential biomarker for gentamicin-induced nephrotoxicity, especially collecting duct cell dysfunction. Gentamicin was given to rats intraperitoneally once every day starting on day 0. Gentamicin significantly increased the plasma creatinine concentration from day 5 and beyond. Also, gentamicin induced polyuria and a defective urine concentration mechanism on day 7, suggesting gentamicin-induced collecting duct cell dysfunction. Immunoblot analysis showed that gentamicin significantly increased urinary exosomal AQP2 excretion on day 1 but decreased it on day 7 compared with the control group. Similarly, increased excretion of exosomal tumor susceptibility gene 101 protein, frequently used as an exosome marker protein, was observed on day 1. However, gentamicin did not significantly affect the urinary excretion of exosomal tumor susceptibility gene 101 on day 7. Gentamicin slightly decreased renal AQP2 expression on day 2 and markedly decreased it on day 8. These data strongly suggest that the use of urinary exosomal AQP2 as a biomarker may allow detection of gentamicin-induced collecting duct cell dysfunction. Furthermore, urinary exosomal AQP2 might also be useful for the early detection of gentamicin-induced renal injury in addition to collecting duct injury.

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Background: Cadmium (Cd) is a well-known hazardous environmental contaminant. It exerts its toxicity through induction of lipid peroxidation and reduction of cellular antioxidant. Therefore, in this study, we investigated whether cinnamon could protect against Cd toxicity in liver and kidney. Materials and methods: Forty male Wister rats (130-135 gm) were divided randomly into 4 groups/ 10 rats each. Control, cinnamon, cadmium, and Cinn+Cd groups received distilled water, cinnamon extract (200 mg/kg b.wt. orally), cadmium chloride (5 mg/kg b.wt. orally), and Cd plus cinnamon, respectively. Blood, liver, and kidney samples were collected after 8 weeks of treatment. Erythrogram, leukogram, liver and kidney functions, and oxidative status (MDA, CAT, and TAC) were determined. Results and discussion: Cd-treated animals showed significant increases in serum ALT, AST, creatinine, and urea indicating hepatic and renal damage. Cd-induced oxidative stress was observed by marked decease TAC accompanied by increase in MDA which contributed in liver and kidney dysfunction. Co-treatment of Cd with cinnamon has improved the oxidation profile by increasing the TAC and decreasing the lipid peroxidation. Cinnamon ameliorated the toxic effect of Cd, which observed by improvement of liver and kidney functions. Conclusion: High antioxidants content of cinnamon could protect the liver and kidney from Cd toxicity.

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