Nath R, Prasad R, Palinal V K, Chopra R K
Prog Food Nutr Sci. 1984;8(1-2):109-63.
Cadmium has been shown to manifest its toxicity in human and animals by mainly accumulating in almost all of the organs and kidney is the main target organ where it is concentrated mainly in cortex. Environmental exposure of cadmium occurs via food, occupational industries, terrestrial and aquatic ecosystem. At molecular level, cadmium interferes with the utilization of essential metals e.g. Ca, Zn, Se, Cr and Fe and deficiencies of these essential metals including protein and vitamins, exaggerate cadmium toxicity, due to its increased absorption through the gut and greater retention in different organs as metallothionein (Cd-Mt). Cadmium transport, across the intestinal and renal brush border membrane vesicles, is carrier mediated and it competes with zinc and calcium. It has been postulated that cadmium shares the same transport system. Cadmium inhibits protein synthesis, carbohydrate metabolism and drug metabolizing enzymes in liver of animals. Chronic environmental exposure of cadmium produces hypertension in experimental animals. Functional changes accompanying cadmium nephropathy include low molecular weight proteinuria which is of tubular origin associated with excess excretion of proteins such as beta 2 microglobulin, metallothionein and high molecular weight proteinuria of glomerular origin (excretion of proteins such as albumin IgG, transferrin etc.). Recent data has shown that metallothionein is more nephrotoxic to animals. Cadmium is also toxic to central nervous system. It causes an alterations of cellular functions in lungs. Cadmium affects both humoral and cell mediated immune response in animals. Cadmium induces metallothionein in liver and kidney but under certain nutritional deficiencies like protein-calorie malnutrition and calcium deficiency, enhanced induction and greater accumulation of cadmium metallothionein has been observed.
镉已被证明在人和动物中表现出毒性，主要是通过在几乎所有器官中蓄积，而肾脏是主要的靶器官，镉主要集中在肾皮质。镉的环境暴露通过食物、职业行业、陆地和水生生态系统发生。在分子水平上，镉会干扰必需金属（如钙、锌、硒、铬和铁）的利用，而这些必需金属（包括蛋白质和维生素）的缺乏会加剧镉的毒性，因为这会导致镉通过肠道的吸收增加，并以金属硫蛋白（镉-金属硫蛋白）的形式在不同器官中潴留更久。镉通过肠和肾刷状缘膜囊泡的转运是载体介导的，它与锌和钙竞争。据推测，镉共用相同的转运系统。镉会抑制动物肝脏中的蛋白质合成、碳水化合物代谢和药物代谢酶。镉的慢性环境暴露会使实验动物产生高血压。镉肾病伴随的功能变化包括低分子量蛋白尿，其起源于肾小管，与β2微球蛋白、金属硫蛋白等蛋白质的过量排泄有关，以及肾小球起源的高分子量蛋白尿（白蛋白、免疫球蛋白G、转铁蛋白等蛋白质的排泄）。最近的数据表明，金属硫蛋白对动物的肾毒性更大。镉对中枢神经系统也有毒性。它会导致肺部细胞功能的改变。镉会影响动物的体液免疫和细胞介导免疫反应。镉会在肝脏和肾脏中诱导金属硫蛋白的产生，但在某些营养缺乏的情况下，如蛋白质-热量营养不良和钙缺乏，会观察到镉金属硫蛋白的诱导增强和蓄积增加。
