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Changes of Carbonyl Stress Parameters in Rats withDiabetes and Rhabdomyolysis

机译:糖尿病和横纹肌溶解大鼠羰基应激参数的变化

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Aim: To investigate the changes of carbonyl stress parameters in rats with combined streptozotocin induced diabetes (STZD, hyperglycemia model) and glycerol stimulated rhabdomyolysis (RM, oxidative stress model). Methodology: RM was induced by glycerol injection and confirmed by changes of heme oxygenase activity, creatine kinase activity, total heme, creatinine, uric acid, urea and bilirubin. STZD was induced by streptozotocin injection and proved by increasing of glucose levels. Carbonyl stress development was determined by total aldehyde levels, TBARS, protein CO group levels, N(6)-Carboxymethyllysine and low-molecular-weight SH groups in blood plasma and liver tissue.Results: A significant increase of carbonyl stress parameters was recorded in RM and STZD rat groups compared with their relative control levels. In animals subjected to the combined induction of RM and STZD, the level of carbonyl stress parameters was lower than that recorded for the STZD and RM groups: total aldehyde levels were decreased in liver resulting in lower TBARS and protein CO group levels. Low-molecular-weight SH groups were increased compared with STZD.Conclusion: Changes of carbonyl stress parameters indicated the significant role of carbonyl stress in diabetes and in rhabdomyolysis. It was demonstrated that combined stimulation of RM and hyperglycemia led to decreasing of carbonyl stress parameters. It can be suggested that these changes in carbonyl stress parameters can be associated with additional initiation of antioxidant defense systems or some compensatory mechanisms.
机译:目的:研究链脲佐菌素合并糖尿病(STZD,高血糖模型)和甘油刺激的横纹肌溶解(RM,氧化应激模型)大鼠中羰基应激参数的变化。方法:通过甘油注射诱导RM,并通过血红素加氧酶活性,肌酸激酶活性,总血红素,肌酐,尿酸,尿素和胆红素的变化证实。 STZD是通过链脲佐菌素注射诱导的,并通过增加葡萄糖水平来证明。羰基应激的产生取决于血浆和肝脏组织中的总醛水平,TBARS,蛋白质CO基团水平,N(6)-羧甲基赖氨酸和低分子量SH基团。结果: RM和STZD大鼠组与它们的相对对照水平相比。在受到RM和STZD联合诱导的动物中,羰基应激参数水平低于STZD和RM组记录的水平:肝脏中的总醛水平降低,导致TBARS和蛋白CO组水平降低。结论:羰基应激参数的变化表明羰基应激在糖尿病和横纹肌溶解中具有重要作用。已经证明,RM和高血糖症的联合刺激导致羰基应激参数的降低。可以认为,羰基应力参数的这些变化可能与抗氧化剂防御系统的其他启动或某些补偿机制有关。

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