Cadmium Toxicity: Insight into Sources, Toxicokinetics, and Effect on Vital Organs and Embryos
Background: Elemental cadmium, cadmium oxide, sulfide, and chloride are resurrected to the atmosphere from both natural and anthropogenic sources. cadmium concentrations in the blood, urine, and kidney cortex are substantially higher in smokers compared to never smokers. Absorbed cadmium accumulates primly in the renal cortex and liver. The pancreas, thyroid, gall-bladder, and testes can also include comparatively high concentrations. Objectives: The current review aimed to highlight on the effect of cadmium chloride on vital organs and embryos. Absorption of cadmium from the lungs is a major source of exposure between smokers and the occupationally exposed. Cadmium accumulates with age even a maximum level is arrived at about age 50. Metallothionein has been identified in the liver, kidneys, duodenum, urine, and blood of animals. It has been postulated that metallothionein passes through the red cell membrane and is transformed to the kidney. Cadmium being a divalent cation is accumulated by transfer mechanisms developed for necessary metals. Cadmium may interact with zinc, iron, magnesium, manganese, calcium, and selenium and cause their secondary disability and so break down metabolism, resulting in the final morphological and functional changes in many organs. Toxicity could result from cadmium (Cd2+) interacting with cellular ingredients until without get into the cell, but by interaction with receptors on their surface. Cadmium forms covalent and ionic bonds with atoms of sulfur, oxygen, and hydrogen present in the sulfhydryl groups, disulfide, carboxyl, imidazole or severally amino compounds present in the cells, causing significant disruption of their homeostasis. The principle target organelle of cadmium is the mitochondria. Symptoms of acute cadmium intoxicating usually appear after 24 hours are shortness of breath, general weakness, fever. It can also cause pulmonary edema, pneumonia and in acute cases, respiratory failure and death. Cadmium accumulates in the renal cortex and induces tubular damage. It may cause nephrotoxicity by procreating free radicals and/or by inducing necrosis, apoptosis, and creatinine increase in plasma and urea increase in the serum. Exposure to cadmium can cause skeletal damage. Cadmium is attached to low bone mineralization, a high rate of fractures, increased osteoporosis, and intense bone pain. It accumulates in the proximal tubular cells, it compresses cellular functions, which may result in reduced transformation among two forms of vitamin D3. This is probably to causes a decrease in calcium absorption and bone mineralization, which in turn may produce osteomalacia. The skeletal effects observed in young rats exposed to cadmium during the period of rapid skeletal growth and teratogenesis or skeletal effects recorded include sirenomelia (fused lower limbs), Amelia (absence of one or more limbs), and retard ossification of the sternum and ribs, dysplasia of facial bones and rear limbs and edema. Cadmium has been shown to be both embryotoxic and teratogenic in a different of animal species. It accumulates in human placenta and its concentration in cord blood increase with maternal exposure. Cadmium may be responsible for decreasing the volume of fetal capillaries in the terminal villi of the placenta. Furthermore, increasing the connective tissue about the fetal vessels changed synthesis of serum and amniotic fluid proteins and decreased expression of growth factors also may key a role in cadmium teratogenicity. Cadmium induces oxidative stress in many organisms at the cellular level, which may outcomes in physiological damage to various organs such as kidneys, liver, lung, pancreas, testes, placenta and bones Cadmium induces oxidative stress in many organisms at the cellular level, which may outcomes in physiological damage to various organs such as kidneys, liver, lung, pancreas, testes, placenta and bones. Reactive oxygen species reacting with polyunsaturated fatty acids of cell membranes initiate lipid peroxidation process that results in modulation of proteins, alteration in membrane components, and this reason the loss of their impartiality and irrevocable damage. Conclusion: It can be concluded that symptoms of acute cadmium intoxicating are shortness of breath, general weakness, fever. pulmonary edema, and pneumonia. Cadmium accumulates with age in the different organs in the body and induces oxidative stress at the cellular level, which may outcomes in physiological damage to various organs such as kidneys, liver, lung, pancreas, testes, placenta, and bones. Reactive oxygen species reacting with polyunsaturated fatty acids of cell membranes initiate lipid peroxidation process that results in modulation of proteins, alteration in membrane components, and this reason the loss of their impartiality and irrevocable damage. Cadmium has been shown to be both embryotoxic and teratogenic in a different of animal species.
Keywords: Cadmium chloride toxicity, Vital organs, Hepatorenal toxicity, Embryos, Animals teratogenic.
