Vincent H K, Powers S K, Stewart D J, Shanely R A, Demirel H, Naito H
Department of Exercise and Sport Sciences, Center for Exercise Science, University of Florida, Gainesville 32611, USA.
Int J Obes Relat Metab Disord. 1999 Jan;23(1):67-74. doi: 10.1038/sj.ijo.0800761.
To determine: 1) whether obesity predisposes the myocardium to oxidative stress as evidenced by higher tissue levels of myocardial lipid peroxidation, and 2) what cellular mechanisms are responsible for this predisposition.
Comparative, descriptive study of the myocardial tissue of lean and obese Fatty Zucker animals.
12 month old lean (-/fa; n = 6; mean body weight = 590 g) and obese (fa/fa; na = 7; mean body weight= 882 g) male Fatty Zucker rats.
Basal lipid peroxidation (assessed using thiobarbituric reactive acid substances (TBARS) and cumene hydroperoxide equivalents), oxidative and antioxidant enzyme activities (citrate synthase (CS), superoxide dismutase (SOD), glutathione peroxidase (GPX) and catalase (CAT), thiol content, heat shock protein expression (HSP72/73) and TBARS concentrations following an iron-mediated challenge in vitro.
Compared to lean, lipid peroxidation was greater (P < 0.05) in the left ventricle (LV) from obese rats as indicated by higher levels of lipid hydroperoxides (mean = 11.48 vs 13.7 cumene hydroperoxide equivalents (CHPE)/mg lipid) and TBARS (mean = 11.1 vs 13.9 nMol/mg lipid.). The activity of the manganese isoform of superoxide dismutase in the LV was higher (P < 0.05) in obese animals, compared to controls (mean = 135 vs 117 U/mg protein). In contrast, LV catalase and glutathione peroxidase activities did not differ (P > 0.05) between groups. Also, LV levels of HSP 72 (inducible) and 73 (constitutive) did not differ (P > 0.05)( between lean and obese animals. Following an iron-stimulated oxidative challenge in vitro, TBARS concentration was significantly greater (P < 0.05) in LV of obese rats compared to the lean (mean = 12.7 vs 16.7 nMol/mg lipid).
These results support the notion that obesity predisposes the myocardium to oxidative stress. However, the postulate that obesity is associated with elevated myocardial antioxidant enzyme activities and HSPs was only partially supported by these findings.
确定：1）肥胖是否会使心肌易受氧化应激影响，表现为心肌脂质过氧化组织水平升高；2）何种细胞机制导致了这种易感性。
对瘦型和肥胖型脂肪 Zucker 动物的心肌组织进行比较性描述性研究。
12 个月大的瘦型（ - /fa；n = 6；平均体重 = 590 g）和肥胖型（fa/fa；n = 7；平均体重 = 882 g）雄性脂肪 Zucker 大鼠。
基础脂质过氧化（使用硫代巴比妥酸反应性酸性物质（TBARS）和氢过氧化异丙苯当量进行评估）、氧化和抗氧化酶活性（柠檬酸合酶（CS）、超氧化物歧化酶（SOD）、谷胱甘肽过氧化物酶（GPX）和过氧化氢酶（CAT））、硫醇含量、热休克蛋白表达（HSP72/73）以及体外铁介导刺激后的 TBARS 浓度。
与瘦型大鼠相比，肥胖大鼠左心室（LV）中的脂质过氧化程度更高（P < 0.05），脂质氢过氧化物水平更高（平均 = 11.48 对 13.7 氢过氧化异丙苯当量（CHPE）/mg 脂质）以及 TBARS 水平更高（平均 = 11.1 对 13.9 nMol/mg 脂质）表明了这一点。与对照组相比，肥胖动物左心室中超氧化物歧化酶锰同工型的活性更高（P < 0.05）（平均 = 135 对 117 U/mg 蛋白质）。相比之下，两组之间左心室过氧化氢酶和谷胱甘肽过氧化物酶的活性没有差异（P > 0.05）。此外，瘦型和肥胖动物之间左心室中 HSP 72（诱导型）和 73（组成型）的水平没有差异（P > 0.05）。在体外铁刺激的氧化应激挑战后，肥胖大鼠左心室中的 TBARS 浓度显著高于瘦型大鼠（P < 0.05）（平均 = 12.7 对 16.7 nMol/mg 脂质）。
这些结果支持肥胖会使心肌易受氧化应激影响这一观点。然而，肥胖与心肌抗氧化酶活性和热休克蛋白升高相关的假设仅部分得到这些发现的支持。
