Hyperlipidaemia in cisplatin-induced nephrotic rats

Abstract

<jats:p> 1 The serum and hepatic lipid concentrations were investigated in rats made nephrotic with a single intraperitoneal injection of cisplatin (6 mg kg<jats:sup>-1</jats:sup> b.wt.). 2 The serum creatinine and urea concentrations were estimated as indices of nephrotoxicity, and the serum total bilirubin level as a liver function test. 3 The fasting serum total cholesterol, triglycerides (TG) and the cholesterol fractions associated with the various lipoproteins, as well as hepatic cholesterol and TG contents were also measured, following 5, 10 and 15 days from the cisplatin treatment. 4 The results revealed that on day 5 both serum creatinine and urea concentrations were significantly (P50.01) increased, indicating the peak of nephrotoxicity, with no injurious effects on the liver as indicated by the unaltered serum bilirubin concentration. 5 The nephrotoxicity was accompanied by significant elevations in serum total cholesterol and TG concentrations by 49 and 42%, respectively, with significant (P50.05) correlations between the serum cholesterol and TG concentrations versus the serum urea (r=0.68 and r=0.60, respectively). 6 Among the estimated lipoproteins, very low density lipoprotein (VLDL) cholesterol was severely increased to more than twofold with no severe changes in LDL or HDL-cholesterol fractions. On day 5 the liver also showed significant accumulation of TG with no change in the cholesterol content. 7 Animals killed 10 or 15 days post-cisplatin treatment had all the perturbed parameters returned to the normal levels. 8 The present results indicated that rats exposed to a single cisplatin injection exhibit acute reversible nephrosis on day 5 which was accompanied by dyslipidaemia and accumulated liver TG. </jats:p>

Protection Effects of Taurine Supplementation against Cisplatin-Induced Nephrotoxicity in Rats

“…These results are in good agreement with those of previous reports [22,23]. Several reports demonstrate different mechanisms involved in the CDDP-induced nephrotoxicity including protein kinase C activation [24], elevation of caspase-3 activity resulting in renal cell apoptosis [25], enhancement of intrarenal synthesis of thromboxane A 2 [26] and dyslipidemia [27].…”

Time dependent effects of gentamicin on the enzymes of carbohydrate metabolism, brush border membrane and oxidative stress in rat kidney tissues

“…1. This implies that BBM was severely damaged and may have been partially effaced/lost in the lumen by toxic GM insult as reported in histological studies (Ali, 1995;Abdel-Gayoum et al, 1999;Abu-Speton and Abdel-Gayoum, 2001). The enzymes and other proteinic components appeared to be dissociated from the membranes, released and accumulated in the lumen and later excreted in the urine as evident from massive enzymuria and proteinuria.…”

Decreased Cyclosporin A Concentrations in the Absorption Phase Using Microemulsion Preconcentrate Formulation in Rats with Cisplatin-Induced Acute Renal Failure

“…Renal dysfunction is often accompanied by hyperlipidemia. [14][15][16] It is considered that hyperlipidemia was induced by a change of hepatic metabolism of cholesterol, and this change is related to bile acid metabolism. In the oral administration study, the absorption rate of the cyclosporin A injection formulation was decreased as well as that of the MEPC formulation, so cyclosporin A might need appropriate bile acids in order to be absorbed in the intestine in spite of the administered formulations.…”