Evaluation of Cisplatin-Induced Nephrotoxicity in Normal and Carnitine Depleted Rat Models

Abstract

The present study was constructed in order to evaluate and modulate some of the nephrotoxic and cardiotoxic side effects of cisplatin. It is a commonly used chemotherapeutic drug with high activity against several solid tumours. One of the major dose- limiting side effects of cisplatin 1s organ-induced toxicities including nephrotoxicity and cardiotoxicity. L-camitine is a naturally occurring quaternary ammonium compound, which is synthesized endogenously and can be derived from dietary sources. Its stores in the body are found in cardiac and skeletal muscle, with the remainder in liver and kidneys.

Any excess is excreted as either free camitine or as an acylcarnitine. Free camitine may be reabsorbed by the kidney and released into the bloodstream.

On the other hand, D-camitine 1s a non-physiological isomer of L-camitine. It induces depletion of camitine when administered intraperitoneally into rats.

One of the major goals of this study is to investigate whether camitine deficiency should be viewed as an additional risk factor in cisplatin-induced nephrotoxicity, and if so, what are the consequences of this condition on kidney and cardiac function. As well as exploring the - potential protective mechanism of L-camitine against cisplatin-induced organ toxicity.