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首页> 外文期刊>The Internet Journal of Endocrinology >Plasma Lipid Peroxidation Zinc And Erythrocyte Cu-Zn Superoxide Dismutase Enzyme Activity In Patients With Type 2 Diabetes Mellitus In Gorgan City (South East Of The Caspian Sea)
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Plasma Lipid Peroxidation Zinc And Erythrocyte Cu-Zn Superoxide Dismutase Enzyme Activity In Patients With Type 2 Diabetes Mellitus In Gorgan City (South East Of The Caspian Sea)

机译:Gorgan市(里海东南部)2型糖尿病患者血浆脂质过氧化锌和红细胞铜锌超氧化物歧化酶的活性

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Diabetes mellitus is a chronic metabolic disorder, which may be associated with the imbalance between protective effect of antioxidants and increased free radical production. Diabetes mellitus can alter the nutritional status of the individual. The aim of this study was to determine the changes of plasma lipid peroxidation , zinc and erythrocyte cu-zn superoxide dismutase activity in patients with type 2 diabetes mellitus and healthy control in Gorgan city. Fifty type 2 patients with diabetes mellitus and 50 people without diabetes were included in this randomized study. None of patients studied had any diabetic complications. The levels of plasma malondialdehyde and zinc from type 2 diabetes mellitus patients (6.24 ± 0.85 nmol / ml and 116.78± 5.51 mg / dl) and control groups (3.63 ± 0.97 nmol / ml and 146.86 ± 9.06 mg / dl) were determined. Erythrocyte Cu-Zn superoxide dismutase activity from patients with diabetes ( 675.34± 60.89 U / g Hb) and control groups (1052.70± 52.76 U / g Hb) were determined. The increased plasma lipid peroxidation and decreased plasma zinc and erythrocyte Cu-Zn superoxide dismutase activity that we observed in patients with type 2 diabetes mellitus may predispose to the development of cardiovascular complications.We propose that diabetic patients may have elevated requirement for antioxidants. Supplementation with zinc and vitamin or dietary free radical scavengers such as vitamins E and C or tomato, orange and etc. have a potential role in boosting antioxidant-related defences and maybe important in patients with diabetes. Introduction Free radicals are highly reactive molecules generated by biochemical redox reactions that occur as a part of normal cell metabolism (1). These unstable species may cause oxidative damage to DNA, carbohydrate, proteins and lipids that are normally counteracted by protective antioxidants. Oxidative defense is provided by a number of enzymes and vitamins, including the vitamin E, vitamin C and glutathione (2,3,4). In times of increased free radical production, individuals may become deficient in these antioxidants. Excessive free radical production or low antioxidant level leads to oxidation of cellular lipids, proteins and nucleic acids, which results in fragmentation and cross-linking. This may ultimately lead to cell death with widespread pathological consequences (5) The imbalance between protective antioxidants (antioxidant defense) and increased free radical production, leading to oxidative damage, is known as oxidative stress. Oxidative stress is caused by a relative overload of oxidants, i.e., reactive oxygen species. This impairs cellular functions and contributes to the pathophysiology of many diseases. Evidence has accumulated suggesting that complications of diabetes seem to be partially mediated by oxidative stress (6,7,8). The function of zinc in the body metabolism is based on its enzymatic affinity, such as a zinc-enzyme complex or Zinc metalloenzyme. In humans and animals, diabetes maybe results in disturbance of these vital trace elements (9). In most mammals, insulin is stored as zinc crystals and is likely secreted in zinc form. Zinc has important role in modulating the immune system, and its dysfunction in diabetes mellitus may be related in part to the status of zinc (10). Lack or inadequate supply of such nutrients produces functional impairment and can result in disease. The clinical significance and evaluation of zinc in regard to different diseases, including diabetes mellitus remains conflicting as well as controversial. Many questions still remain unanswered. Several reports underscore the role of micronutrient status in patients with type 1 or 2 diabetes mellitus (11,12,13,14,15,16,17). Zinc maybe act in normalizing glycemia, and a restored zinc status in patients with type 2 diabetes mellitus may counteract the deleterious effects of oxidative stress, helping to prevent many complications associated with diabetes. Diabetes mellitus is a ma
机译:糖尿病是一种慢性代谢性疾病,可能与抗氧化剂的保护作用和自由基产生增加之间的不平衡有关。糖尿病可以改变个体的营养状况。这项研究的目的是确定Gorgan市2型糖尿病患者和健康对照者血浆脂质过氧化,锌和红细胞cu-zn超氧化物歧化酶活性的变化。这项随机研究包括50例2型糖尿病患者和50例非糖尿病患者。研究的患者均无糖尿病并发症。测定2型糖尿病患者的血浆丙二醛和锌水平(6.24±0.85 nmol / ml和116.78±5.51 mg / dl)和对照组(3.63±0.97 nmol / ml和146.86±9.06 mg / dl)。测定了糖尿病患者(675.34±60.89 U / g Hb)和对照组(1052.70±52.76 U / g Hb)的红细胞Cu-Zn超氧化物歧化酶活性。我们在2型糖尿病患者中观察到的血浆脂质过氧化作用的增加以及血浆锌和红细胞铜锌超氧化物歧化酶活性的降低可能是心血管并发症的诱因。我们建议糖尿病患者对抗氧化剂的需求可能增加。补充锌和维生素或饮食中的自由基清除剂,例如维生素E和C或番茄,橙子等,对增强抗氧化剂相关的防御能力具有潜在作用,对糖尿病患者可能很重要。简介自由基是由生物化学氧化还原反应产生的高反应性分子,是正常细胞代谢的一部分(1)。这些不稳定的物质可能会导致DNA,碳水化合物,蛋白质和脂质的氧化损伤,这些通常被保护性抗氧化剂所抵消。多种酶和维生素可提供氧化防御作用,包括维生素E,维生素C和谷胱甘肽(2,3,4)。在自由基产生增加的时期,个体可能缺乏这些抗氧化剂。自由基产生过多或抗氧化剂含量低会导致细胞脂质,蛋白质和核酸氧化,从而导致断裂和交联。这最终可能导致细胞死亡,并带来广泛的病理后果(5)保护性抗氧化剂(抗氧化剂防御)与自由基产生增加之间的不平衡,导致氧化损伤,被称为氧化应激。氧化应力是由相对过量的氧化剂(即活性氧)引起的。这损害细胞功能,并有助于许多疾病的病理生理。越来越多的证据表明,糖尿病并发症似乎部分是由氧化应激介导的(6,7,8)。锌在人体新陈代谢中的功能基于其酶亲和力,例如锌酶复合物或锌金属酶。在人类和动物中,糖尿病可能导致这些重要微量元素的紊乱(9)。在大多数哺乳动物中,胰岛素以锌晶体的形式存储,并可能以锌形式分泌。锌在调节免疫系统中起重要作用,其在糖尿病中的功能障碍可能部分与锌的状态有关(10)。这些营养素的缺乏或不足会导致功能受损,并可能导致疾病。锌在包括糖尿病在内的不同疾病方面的临床意义和评估仍然存在矛盾和争议。许多问题仍然没有答案。一些报告强调微量营养素状态在1型或2型糖尿病患者中的作用(11,12,13,14,15,16,17)。锌可能起到使血糖正常化的作用,而2型糖尿病患者中锌的恢复状态可以抵消氧化应激的有害影响,有助于预防许多与糖尿病相关的并发症。糖尿病是一种疾病

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