Tinkov Alexey A, Ajsuvakova Olga P, Skalnaya Margarita G, Popova Elizaveta V, Sinitskii Anton I, Nemereshina Olga N, Gatiatulina Evgenia R, Nikonorov Alexandr A, Skalny Anatoly V
Laboratory of Biotechnology and Applied Bioelementology, Yaroslavl State University, Sovetskaya st., 14, Yaroslavl, 150000, Russia,
Biometals. 2015 Apr;28(2):231-54. doi: 10.1007/s10534-015-9823-2. Epub 2015 Jan 30.
A significant interrelation between heavy metal exposure and metabolic syndrome (MetS) development has been demonstrated earlier. Despite the presence of a number of works aimed at the investigation of the role of Hg in MetS development, the existing data remain contradictory. Therefore, the primary objective of the current work is to review the existing data regarding the influence of mercury on universal mechanisms involved in the pathogenesis of the development of MetS and its components. The brief chemical characterization of mercury is provided. The role of mercury in induction of oxidative stress has been discussed. In particular, Hg-induced oxidative stress may occur due to both prooxidant action of the metal and decrease in antioxidant enzymes. Despite the absence of direct indications, it can be proposed that mercury may induce endoplasmic reticulum stress. As it is seen from both in vivo and in vitro studies, mercury is capable of inducing inflammation. The reviewed data demonstrate that mercury affects universal pathogenetic mechanisms of MetS development. Moreover, multiple investigations have indicated the role of mercury in pathogenesis of MetS components: dyslipidemia, hypertension, insulin resistance, and obesity to a lesser extent. The present state of data regarding the interrelation between mercury and MetS denotes the following perspectives: (1) Further clinic-epidemiologic and experimental studies are required to estimate the association between mercury exposure and the development of MetS components, especially obesity; (2) Additional investigations of the possible effect of organism's mercury content modulation on MetS pathogenesis should be undertaken.
此前已有研究表明重金属暴露与代谢综合征（MetS）的发生发展之间存在显著的相互关系。尽管有许多旨在研究汞在MetS发生发展中作用的研究，但现有数据仍相互矛盾。因此，本研究的主要目的是回顾现有关于汞对参与MetS发生发展及其组分发病机制的普遍机制影响的数据。文中提供了汞的简要化学特性。讨论了汞在诱导氧化应激中的作用。特别是，汞诱导的氧化应激可能由于金属的促氧化作用和抗氧化酶的减少而发生。尽管没有直接证据，但可以推测汞可能诱导内质网应激。从体内和体外研究都可以看出，汞能够诱导炎症。综述数据表明汞影响MetS发生发展的普遍发病机制。此外，多项研究表明汞在MetS组分的发病机制中起作用：血脂异常、高血压、胰岛素抵抗，在肥胖方面作用较小。关于汞与MetS之间相互关系的现有数据现状表明了以下几个方面：（1）需要进一步开展临床流行病学和实验研究，以评估汞暴露与MetS组分发生发展之间的关联，尤其是肥胖；（2）应进一步研究调节机体汞含量对MetS发病机制的可能影响。
