摘要
在最重要的生理功能中,细胞氧化还原平衡的维持是一个主要的稳态事件。许多环境污染物有效的套住了细胞还原化合物,但是这种毒性模式的实际重要性还远不为人所知。这种情况出现在一些慢性发展的长期疾病案例中,如神经退行性病,糖尿病和许多其他的疾病。糖尿病中氧化困难的介入被认为与长期 饮食暴露于低浓度镉有关联。与多氯联苯分子(PCB)比较:他们在结构上与镉无关联,他们比镉优先分配到不同的器官,他们遵从不同的代谢途径。然而,他们也有促氧化性质,他们与糖尿病有联系。既然镉和多氯联苯都不是准确的氧化剂,他们都遵循不同的方式来移动氧化还原平衡。因此,机体的适应性反应一定会产生差别,如抗氧化反应,氧化物种产生的不可逆损伤,又如,当暴露在低浓度时发生的氧化损伤。从可用的相关数据中预计了暴露的高低浓度的大概界线,并阐述了实验模型的强弱度。最终,长期暴露于低浓度的污染物中造成功能失调和疾病的细胞反应前兆,例如糖尿病:氧化损伤是一个伴随现象且在毒性的早期机制中是不必要的。
关键词: 镉,糖尿病,胰岛素,氧化应激,多氯联苯化合物,低剂量,生物标记物,风险评价
图形摘要
Current Drug Targets
Title:Chronic Exposure to Low-Level Cadmium in Diabetes: Role of Oxidative Stress and Comparison with Polychlorinated Biphenyls
Volume: 17 Issue: 12
Author(s): Adeline Jacquet, Fayçal Ounnas, Marine Lénon, Josiane Arnaud, Christine Demeilliers, Jean-Marc Moulis
Affiliation:
关键词: 镉,糖尿病,胰岛素,氧化应激,多氯联苯化合物,低剂量,生物标记物,风险评价
摘要: Among the most important physiological functions, maintenance of the oxidation reduction equilibrium in cells stands out as a major homeostatic event. Many environmental contaminants efficiently trap cellular reducing compounds, but the actual importance of this mode of toxicity is far from being precisely known. This statement applies to cases of slowly developing chronic diseases, such as neurodegenerations, diabetes, and many others. The involvement of oxidative challenge in diabetes is considered in connection with chronic dietary exposure to low-level concentrations of cadmium. Comparison is made with polychlorobiphenyl molecules (PCB): they are structurally unrelated to cadmium, they preferentially distribute into different organs than cadmium, and they follow different metabolic pathways. Yet, they have also pro-oxidative properties, and they are associated with diabetes. Since neither cadmium nor PCB is a direct oxidant, they both follow indirect pathways to shift the redox equilibrium. Thus, a difference must be made between the adaptable response of the organism, i.e. the anti-oxidant response, and the irreversible damage generated by oxidizing species, i.e. oxidative damage, when exposure occurs at low concentrations. The approximate border between high and low levels of exposure is estimated in this review from the available relevant data, and the strengths and weaknesses of experimental models are delineated. Eventually, chronic low level exposure to these contaminants sparks cellular responses setting ground for dysfunction and disease, such as diabetes: oxidative damage is an accompanying phenomenon and not necessarily an early mechanism of toxicity.
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Cite this article as:
Adeline Jacquet, Fayçal Ounnas, Marine Lénon, Josiane Arnaud, Christine Demeilliers, Jean-Marc Moulis , Chronic Exposure to Low-Level Cadmium in Diabetes: Role of Oxidative Stress and Comparison with Polychlorinated Biphenyls, Current Drug Targets 2016; 17 (12) . https://dx.doi.org/10.2174/1389450116666150531151228
DOI https://dx.doi.org/10.2174/1389450116666150531151228 |
Print ISSN 1389-4501 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-5592 |
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