Department of Medicine, Vanderbilt University School of Medicine, Division of Human Nutrition, Saint Thomas Medical Group, Saint Thomas Hospital, Nashville, TN, USA.
J Clin Hypertens (Greenwich). 2011 Aug;13(8):621-7. doi: 10.1111/j.1751-7176.2011.00489.x. Epub 2011 Jul 11.
Mercury has a high affinity for sulfhydryl groups, inactivating numerous enzymatic reactions, amino acids, and sulfur-containing antioxidants (N-acetyl-L-cysteine, alpha-lipoic acid, L-glutathione), with subsequent decreased oxidant defense and increased oxidative stress. Mercury binds to metallothionein and substitute for zinc, copper, and other trace metals, reducing the effectiveness of metalloenzymes. Mercury induces mitochondrial dysfunction with reduction in adenosine triphosphate, depletion of glutathione, and increased lipid peroxidation. Increased oxidative stress and reduced oxidative defense are common. Selenium and fish containing omega-3 fatty acids antagonize mercury toxicity. The overall vascular effects of mercury include increased oxidative stress and inflammation, reduced oxidative defense, thrombosis, vascular smooth muscle dysfunction, endothelial dysfunction, dyslipidemia, and immune and mitochondrial dysfunction. The clinical consequences of mercury toxicity include hypertension, coronary heart disease, myocardial infarction, cardiac arrhythmias, reduced heart rate variability, increased carotid intima-media thickness and carotid artery obstruction, cerebrovascular accident, generalized atherosclerosis, and renal dysfunction, insufficiency, and proteinuria. Pathological, biochemical, and functional medicine correlations are significant and logical. Mercury diminishes the protective effect of fish and omega-3 fatty acids. Mercury inactivates catecholaminei-0-methyl transferase, which increases serum and urinary epinephrine, norepinephrine, and dopamine. This effect will increase blood pressure and may be a clinical clue to mercury-induced heavy metal toxicity. Mercury toxicity should be evaluated in any patient with hypertension, coronary heart disease, cerebral vascular disease, cerebrovascular accident, or other vascular disease. Specific testing for acute and chronic toxicity and total body burden using hair, toenail, urine, and serum should be performed.
汞对巯基具有很高的亲和力，会使许多酶反应、氨基酸和含硫抗氧化剂（N-乙酰-L-半胱氨酸、α-硫辛酸、L-谷胱甘肽）失活，随后降低氧化防御能力并增加氧化应激。汞与金属硫蛋白结合并替代锌、铜和其他微量元素，降低金属酶的有效性。汞会导致线粒体功能障碍，减少三磷酸腺苷，耗尽谷胱甘肽，并增加脂质过氧化。氧化应激增加和氧化防御降低是常见的。硒和含有欧米伽-3 脂肪酸的鱼能拮抗汞的毒性。汞对血管的总体影响包括增加氧化应激和炎症、降低氧化防御、血栓形成、血管平滑肌功能障碍、内皮功能障碍、血脂异常以及免疫和线粒体功能障碍。汞毒性的临床后果包括高血压、冠心病、心肌梗死、心律失常、心率变异性降低、颈动脉内膜中层厚度增加和颈动脉阻塞、脑血管意外、全身性动脉粥样硬化以及肾功能不全、衰竭和蛋白尿。病理、生化和功能医学相关性具有重要意义且合乎逻辑。汞会减弱鱼和欧米伽-3 脂肪酸的保护作用。汞会使儿茶酚胺-O-甲基转移酶失活，增加血清和尿液中的肾上腺素、去甲肾上腺素和多巴胺。这种作用会增加血压，可能是汞引起重金属毒性的临床线索。任何患有高血压、冠心病、脑血管疾病、脑血管意外或其他血管疾病的患者都应评估汞毒性。应使用头发、指甲、尿液和血清进行急性和慢性毒性以及全身负荷的特定检测。
