阿斯巴甜诱导白化大鼠免疫器官电解质稳态的改变

Arbind Kumar Choudhary, Sheela Devi Rathinasamy
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引用次数: 7

摘要

阿斯巴甜在人类和实验动物体内被迅速和完全代谢为天冬氨酸(40%)、苯丙氨酸(50%)和甲醇(10%)。甲醇是一种有毒的代谢物,主要通过氧化代谢为甲醛,然后生成甲酸盐。这些过程伴随着超氧阴离子和过氧化氢的形成。本研究旨在了解口服阿斯巴甜(40 mg/kg bw) 15天、30天和90天对免疫器官是否有任何影响。通过膜结合atp酶的水平来评估对质膜的损伤。通过脂质过氧化物、蛋白质羰基、蛋白质硫醇和脂溶性抗氧化剂维生素e水平的变化来评估氧化应激状态。为了模拟人类甲醇代谢,研究人员使用叶酸缺乏的动物。免疫器官各膜结合atp酶活性均降低。大鼠给药阿斯巴甜诱导过量自由基生成,证实了脂质过氧化增加,这一明显现象在本研究中也再次得到了蛋白羰基升高和蛋白硫醇降低的证实。这些过量的自由基也会降低免疫器官的细胞数量(器官重量和细胞数量的减少)。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Aspartame induces alteration in electrolytes homeostasis of immune organs in wistar albino rats

Aspartame is rapidly and completely metabolized in humans and experimental animals to aspartic acid (40%), phenylalanine (50%) and methanol (10%). Methanol, a toxic metabolite is primarily metabolized by oxidation to formaldehyde and then to formate. These processes are accompanied by the formation of superoxide anion and hydrogen peroxide. This study is focused to understand whether the oral administration of Aspartame (40 mg/kg bw) for 15 days, 30 days, and 90 days have any effect on immune organs. Damage to plasma membrane was assessed by levels of membrane-bound ATPases. Oxidative stress status was assessed by alterations in level of lipid peroxides, protein carbonyls, protein thiol and lipid-soluble antioxidant vitamin E. To mimic human methanol metabolism, folate-deficient animals were used. There was decrease in all membrane-bound ATPases activities in immune organs. Aspartame administration to rats inducing excess free radical generation is confirmed by increase in lipid peroxidation, obvious which is also again substantiated by the elevated protein carbonyl and decrease in protein thiol in this study. These excess free radical generations also decrease the cellularity (reduction in organ weight and cell count) of immune organs.

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