OBJECTIVE Some factors related to lifestyle, including stress and high-fat diet (HFD) consumption, are associated with higher prevalence of obesity. These factors can lead to an imbalance between ROS production and antioxidant defenses and to mitochondrial dysfunctions, which, in turn, could cause metabolic impairments, favoring the development of obesity. However, little is known about the interplay between these factors, particularly at early ages, and whether long-term sex-specific changes may occur. Here, we evaluated whether social isolation during the prepubertal period only, associated or not with chronic HFD, can exert long-term effects on oxidative status parameters and on mitochondrial function in the whole hypothalamus, in a sex-specific manner. METHODS Wistar male and female rats were divided into two groups (receiving standard chow or standard chow + HFD), that were subdivided into exposed or not to social isolation during the prepubertal period. Oxidative status parameters, and mitochondrial function were evaluated in the hypothalamus in the adult age. RESULTS Regarding antioxidant enzymes activities, HFD decreased GPx activity in the hypothalamus, while increasing SOD activity in females. Females also presented increased total thiols; however, non-protein thiols were lower. Main effects of stress and HFD were observed in TBARS levels in males, with both factors decreasing this parameter. Additionally, HFD increased complex IV activity, and decreased mitochondrial mass in females. Complex I-III activity was higher in males compared to females. CONCLUSION Stress during the prepubertal period and chronic consumption of HFD had persistent sex-specific effects on oxidative status, as well as on its consequences for the cell and for mitochondrial function. HFD had more detrimental effects on females, inducing oxidative imbalance, which resulted in damage to the mitochondria. This HFD-induced imbalance may be related to the development of obesity.

中文翻译：

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青春期前应激和获得高脂饮食对下丘脑线粒体和氧化应激参数的性别依赖性影响。

目的与生活方式有关的一些因素，包括压力和高脂饮食（HFD）的消耗，与肥胖的患病率较高有关。这些因素可导致ROS产生与抗氧化剂防御之间的不平衡，以及线粒体功能障碍，进而导致代谢障碍，有利于肥胖症的发展。但是，人们对这些因素之间的相互作用（尤其是在幼年时期）以及是否可能发生长期的性别特异性变化知之甚少。在这里，我们评估了是否仅在青春期前进行社会隔离，无论是否与慢性HFD相关，都可以以性别特定的方式对整个下丘脑的氧化状态参数和线粒体功能产生长期影响。方法Wistar雄性和雌性大鼠分为两组（接受标准食物或标准食物+ HFD），在青春期前被分为暴露或未进行社会隔离。在成年年龄的下丘脑中评估了氧化状态参数和线粒体功能。结果关于抗氧化酶活性，HFD降低了下丘脑的GPx活性，同时增加了女性的SOD活性。女性的总硫醇含量也有所增加。然而，非蛋白质硫醇含量较低。在男性的TBARS水平中观察到了压力和HFD的主要影响，而这两个因素均降低了该参数。另外，HFD增加了女性的复杂IV活性，并降低了线粒体质量。与女性相比，男性的复杂I-III活性更高。结论青春期前的压力和HFD的长期服用对氧化状态及其对细胞和线粒体功能的后果具有持续的性别特异性影响。HFD对女性具有更大的有害作用，导致氧化不平衡，从而导致线粒体受损。这种由HFD引起的失衡可能与肥胖的发展有关。