Houston Mark C
Vanderbilt University School of Medicine, USA.
Altern Ther Health Med. 2007 Mar-Apr;13(2):S128-33.
Mercury, cadmium, and other heavy metals have a high affinity for sulfhydryl (-SH) groups, inactivating numerous enzymatic reactions, amino acids, and sulfur-containing antioxidants (NAC, ALA, GSH), with subsequent decreased oxidant defense and increased oxidative stress. Both bind to metallothionein and substitute for zinc, copper, and other trace metals reducing the effectiveness of metalloenzymes. Mercury induces mitochondrial dysfunction with reduction in ATP, depletion of glutathione, and increased lipid peroxidation; increased oxidative stress is common. Selenium antagonizes mercury toxicity. The overall vascular effects of mercury include oxidative stress, inflammation, thrombosis, vascular smooth muscle dysfunction, endothelial dysfunction, dyslipidemia, immune dysfunction, and mitochondrial dysfunction. The clinical consequences of mercury toxicity include hypertension, CHD, MI, increased carotid IMT and obstruction, CVA, generalized atherosclerosis, and renal dysfunction with proteinuria. Pathological, biochemical, and functional medicine correlations are significant and logical. Mercury diminishes the protective effect of fish and omega-3 fatty acids. Mercury, cadmium, and other heavy metals inactivate COMT, which increases serum and urinary epinephrine, norepinephrine, and dopamine. This effect will increase blood pressure and may be a clinical clue to heavy metal toxicity. Cadmium concentrates in the kidney, particularly inducing proteinuria and renal dysfunction; it is associated with hypertension, but less so with CHD. Renal cadmium reduces CYP4A11 and PPARs, which may be related to hypertension, sodium retention, glucose intolerance, dyslipidemia, and zinc deficiency. Dietary calcium may mitigate some of the toxicity of cadmium. Heavy metal toxicity, especially mercury and cadmium, should be evaluated in any patient with hypertension, CHD, or other vascular disease. Specific testing for acute and chronic toxicity and total body burden using hair, toenail, urine, serum, etc. with baseline and provoked evaluation should be done.
汞、镉和其他重金属对巯基（-SH）具有高度亲和力，会使众多酶促反应、氨基酸和含硫抗氧化剂（N-乙酰半胱氨酸、α-硫辛酸、谷胱甘肽）失活，进而导致氧化防御能力下降和氧化应激增加。两者都会与金属硫蛋白结合并取代锌、铜和其他微量元素，从而降低金属酶的效能。汞会导致线粒体功能障碍，表现为三磷酸腺苷（ATP）减少、谷胱甘肽耗竭以及脂质过氧化增加；氧化应激增加很常见。硒可拮抗汞的毒性。汞对血管的总体影响包括氧化应激、炎症、血栓形成、血管平滑肌功能障碍、内皮功能障碍、血脂异常、免疫功能障碍和线粒体功能障碍。汞中毒的临床后果包括高血压、冠心病、心肌梗死、颈动脉内膜中层厚度增加及阻塞、脑血管意外、全身性动脉粥样硬化以及伴有蛋白尿的肾功能障碍。病理、生化和功能医学之间的关联显著且合理。汞会削弱鱼类和ω-3脂肪酸的保护作用。汞、镉和其他重金属会使儿茶酚-O-甲基转移酶（COMT）失活，从而增加血清和尿液中的肾上腺素、去甲肾上腺素和多巴胺。这种作用会升高血压，可能是重金属中毒的一个临床线索。镉在肾脏中蓄积，尤其会导致蛋白尿和肾功能障碍；它与高血压有关，但与冠心病的关联较小。肾脏中的镉会降低细胞色素P450 4A11（CYP4A11）和过氧化物酶体增殖物激活受体（PPARs），这可能与高血压、钠潴留、葡萄糖耐量异常、血脂异常和锌缺乏有关。膳食钙可能会减轻镉的一些毒性。对于任何患有高血压、冠心病或其他血管疾病的患者，都应评估重金属中毒情况，尤其是汞和镉中毒。应使用头发、趾甲、尿液、血清等进行急性和慢性毒性以及全身负荷的特异性检测，并进行基线和激发评估。
