Dept. of Zoology, Faculty of Science, Annamalai Univ., Annamalainagar 608 002, Tamil Nadu, India.
J Food Sci. 2010 Sep;75(7):T132-40. doi: 10.1111/j.1750-3841.2010.01757.x.
Cadmium (Cd) exposure results in numerous pathological consequences including oxidative stress and dyslipidemia. The present study was designed to investigate the efficacy of combined treatment with quercetin (QE) and α-tocopherol (AT) against Cd-induced oxidative stress and alterations in lipids and lipoproteins in the plasma and liver of rats. Oral administration of Cd (5 mg/kg bw/d) for 4 wk has shown a significant (P < 0.05) increase in thiobarbituric acid reactive substances (TBARS), lipid hydro peroxides (LOOH), total cholesterol, low density lipoprotein cholesterol (LDL-C), very low density lipoprotein cholesterol (VLDL-C), free fatty acids (FFA), phospholipids (PL), triglycerides (TGs), and the activity of hydroxyl-3-methylglutaryl-coenzyme A reductase (HMG-CoA reductase) in plasma with a significant (P > 0.05) reduction in the levels of reduced glutathione (GSH), high density lipoprotein cholesterol (HDL-C), and the activity of lecithin cholesterol acyl transferase (LCAT) in plasma. In addition, the levels of hepatic thiobarbituric acid reactive substances (TBARS), LOOH, conjugated dienes (CD), protein carbonyls (PC), and the activity of HMG-CoA reductase, levels of cholesterol, FFA, and TGs were significantly (P > 0.05) increased and the level of PL is significantly (P > 0.05) decreased along with the decreased activity of LCAT in the liver of Cd-treated rats. Oral supplementation with QE (50 mg/kg bw/d) and AT (50 mg/kg bw/d) for 4 wk in Cd intoxicated rats significantly (P > 0.05) has reduced the plasma levels of TBARS, LOOH, GSH, cholesterol, FFA, TGs, VLDL-C, LDL-C, and the activity of HMG-CoA and significantly (P > 0.05) has increased the activity of LCAT and the plasma levels of HDL-C. The oral supplementation also significantly (P > 0.05) has reduced the hepatic oxidative stress markers, cholesterol, TGs, FFA, and significantly (P > 0.05) has increased the LCAT activity and the PL in liver. Our results indicate that the combined treatment with QE and AT has normalized all the previously mentioned biochemical parameters in Cd-intoxicated rats than the individual treatments. The combined treatment has provided remarkable protection against Cd-induced oxidative stress and alterations in lipid metabolism and, thereby, reduced the Cd-mediated cardiovascular diseases.
镉(Cd)暴露会导致许多病理后果,包括氧化应激和血脂异常。本研究旨在探讨槲皮素(QE)和α-生育酚(AT)联合治疗对大鼠血浆和肝脏中镉诱导的氧化应激和脂质及脂蛋白变化的疗效。口服给予 Cd(5mg/kg bw/d)4 周后,血浆中硫代巴比妥酸反应物质(TBARS)、脂质过氧化物(LOOH)、总胆固醇、低密度脂蛋白胆固醇(LDL-C)、极低密度脂蛋白胆固醇(VLDL-C)、游离脂肪酸(FFA)、磷脂(PL)、甘油三酯(TGs)和羟甲基戊二酸单酰辅酶 A 还原酶(HMG-CoA 还原酶)的活性显著增加(P<0.05),而血浆中还原型谷胱甘肽(GSH)、高密度脂蛋白胆固醇(HDL-C)和卵磷脂胆固醇酰基转移酶(LCAT)的活性显著降低(P>0.05)。此外,肝组织中 TBARS、LOOH、共轭二烯(CD)、蛋白羰基(PC)和 HMG-CoA 还原酶的活性、胆固醇、FFA 和 TGs 的水平显著增加(P>0.05),而 LCAT 的活性降低,导致肝组织中 PL 的水平显著降低(P>0.05)。在 Cd 中毒大鼠中,连续 4 周口服补充 QE(50mg/kg bw/d)和 AT(50mg/kg bw/d)可显著降低血浆 TBARS、LOOH、GSH、胆固醇、FFA、TGs、VLDL-C、LDL-C 和 HMG-CoA 活性(P>0.05),并显著升高 LCAT 活性和 HDL-C 水平(P>0.05)。口服补充还可显著降低肝组织氧化应激标志物、胆固醇、TGs、FFA 的水平(P>0.05),显著升高 LCAT 活性和 PL 的水平(P>0.05)。我们的结果表明,与单独治疗相比,QE 和 AT 的联合治疗使 Cd 中毒大鼠的所有上述生化参数恢复正常。联合治疗对 Cd 诱导的氧化应激和脂质代谢变化具有显著的保护作用,从而降低了 Cd 介导的心血管疾病的发生风险。