Background:Oxidative damage contributes to the pathophysiology of schizophrenia (SZ). Redox imbalance maylead to increased lipid peroxidation, which produces toxic aldehydes like 4-hydroxynonenal (4-HNE) ultimately leading tooxidative stress. Conversely, implications of oxidative stress points towards an alteration in HNE-protein adducts andactivities of enzymatic and antioxidant systems in schizophrenia.Objectives:Present study focuses on identification of HNE-protein adducts and its related molecular consequences inschizophrenia pathology due to oxidative stress, particularly lipid peroxidation.Material and Methods: Oxyblotting was performed on seven autopsied brain samples each from cortex and hippocampusregion of schizophrenia patients and their respective normal healthy controls. Additionally, thiobarbituric acid substances(TBARS), reduced glutathione (GSH) levels and catalase (CAT) activities associated with oxidative stress, were alsoestimated.Results:Obtained results indicates substantially higher levels of oxidative stress in schizophrenia patients than healthycontrol group represented by elevated expression of HNE-protein adducts. Interestingly, hippocampus region ofschizophrenia brain shows increased HNE protein adducts compared to cortex. An increase in catalase activity (4.8876 ±1.7123) whereas decrease in antioxidant GSH levels (0.213 ± 0.015µmol/ml) have been observed in SZ brain. ElevatedTBARS level (0.3801 ± 0.0532ug/ml) were obtained in brain regions SZ patients compared with their controls that reflectsan increased lipid peroxidation (LPO).Conclusion:Conclusion: We propose the role of HNE modified proteins possibly associated with the pathology ofschizophrenia. Our data revealed increase lipid peroxidation as a consequence of increased TBARS production.Furthermore, altered cellular antioxidants pathways related to GSH and CAT also highlight the involvement of oxidativestress in schizophrenia pathology.

中文翻译：

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4-羟基壬烯醛修饰蛋白在精神分裂症脑中的表达分析；与参与氧化还原失调的相关性

背景：氧化损伤有助于精神分裂症（SZ）的病理生理学。氧化还原失衡可能导致脂质过氧化增加，从而产生有毒醛类，如 4-羟基壬烯醛 (4-HNE)，最终导致氧化应激。相反，氧化应激的影响指向精神分裂症中 HNE 蛋白加合物和酶促和抗氧化系统活性的改变。过氧化。材料和方法：对来自精神分裂症患者及其各自的正常健康对照的皮质和海马区的七个尸检脑样本进行氧印迹。此外，硫代巴比妥酸物质（TBARS），还估计了与氧化应激相关的谷胱甘肽 (GSH) 水平和过氧化氢酶 (CAT) 活性降低。结果：获得的结果表明，精神分裂症患者的氧化应激水平显着高于健康对照组，表现为 HNE 蛋白加合物的表达升高。有趣的是，与皮质相比，精神分裂症大脑的海马区显示出增加的 HNE 蛋白加合物。在 SZ 脑中观察到过氧化氢酶活性增加 (4.8876 ±1.7123) 而抗氧化剂 GSH 水平降低 (0.213 ± 0.015µmol/ml)。与对照组相比，SZ患者脑区TBARS水平升高（0.3801±0.0532ug/ml），反映脂质过氧化（LPO）增加。结论：结论：我们提出HNE修饰蛋白的作用可能与精神分裂症的病理有关。