Bone mineral health is sensitively related to environmental cadmium exposure- experimental and human data

Buha, Aleksandra; Jugdaohsingh, Ravin; Matović, Vesna; Bulat, Zorica; Antonijević, Biljana; Kerns, Jemma G.; Goodship, Allen E.; Hart, Alister; Powell, Jonathan J.

doi:10.1016/j.envres.2019.108539

Cited by 67 publications

(37 citation statements)

References 57 publications

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“…Recent work has shown that lower iron content in females than in males may be due to their different physiologies, which may allow for greater absorption of Cd by the female gastrointestinal tract [38,39]. The suggestion in this study that females may be more sensitive to Cd-induced nephrotoxicity than males supports an earlier study [40,41].…”

Section: Discussionsupporting

confidence: 85%

An assessment of sensitivity biomarkers for urinary cadmium burden

Wang

et al. 2020

BMC Nephrol

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Background: Excess cadmium (Cd) intake poses a general risk to health and to the kidneys in particular. Among indices of renal dysfunction under Cd burden measures are the urinary N-acetyl-β-D-glucosidase (UNAG) and urinary β 2-microglobulin (Uβ 2-MG) enzymes. However, the end-pointed values and the Cd burden threshold remain controversial because the scopes fluctuate widely. Methods: To ascertain the clinical benchmark dose of urinary Cd (UCd) burden for renal dysfunction, 1595 residents near a Cd site were surveyed. Urine was sampled and assayed. A benchmark dose low (BMDL) was obtained by fitting UCd levels and index levels. Results: We found that over 50% of the subjects were suffering from Cd exposure as their UCd levels far exceeded the national standard threshold of 5.000 μg/g creatinine (cr). Further analysis indicated that Uβ 2-MG was more sensitive than UNAG for renal dysfunction. The BMDL for UCd was estimated as 3.486 U/g cr (male, where U is unit of enzyme) and 2.998 U/g cr (female) for UNAG. The BMDL for Uβ 2-MG, which is released into urine from glomerulus after Cd exposure, was found to be 2.506 μg/g cr (male, where μg is the unit of microglobulin) and 2.236 μg/g cr (female). Conclusions: Uβ 2-MG is recommended as the sensitivity index for renal dysfunction, with 2.2 μg/g cr as the threshold for clinical diagnosis. Our findings suggest that Uβ 2-MG is the better biomarker for exposure to Cd.

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Section: Discussionsupporting

confidence: 85%

An assessment of sensitivity biomarkers for urinary cadmium burden

Wang

et al. 2020

BMC Nephrol

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“…The mechanisms of Cd toxicity are various and include binding to SH groups, oxidative stress induction [77,78], interactions with bioelements [79,80,81,82], mitochondrial toxicity [83], and altered microRNA expression [84].…”

Section: Exposure and Effectsmentioning

confidence: 99%

A Review on Coordination Properties of Thiol-Containing Chelating Agents Towards Mercury, Cadmium, and Lead

et al. 2019

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The present article reviews the clinical use of thiol-based metal chelators in intoxications and overexposure with mercury (Hg), cadmium (Cd), and lead (Pb). Currently, very few commercially available pharmaceuticals can successfully reduce or prevent the toxicity of these metals. The metal chelator meso-2,3-dimercaptosuccinic acid (DMSA) is considerably less toxic than the classical agent British anti-Lewisite (BAL, 2,3-dimercaptopropanol) and is the recommended agent in poisonings with Pb and organic Hg. Its toxicity is also lower than that of DMPS (dimercaptopropane sulfonate), although DMPS is the recommended agent in acute poisonings with Hg salts. It is suggested that intracellular Cd deposits and cerebral deposits of inorganic Hg, to some extent, can be mobilized by a combination of antidotes, but clinical experience with such combinations are lacking. Alpha-lipoic acid (α-LA) has been suggested for toxic metal detoxification but is not considered a drug of choice in clinical practice. The molecular mechanisms and chemical equilibria of complex formation of the chelators with the metal ions Hg2+, Cd2+, and Pb2+ are reviewed since insight into these reactions can provide a basis for further development of therapeutics.

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“…Whole-blood and urinary Cd concentrations are widely accepted markers of Cd exposure and accumulation [ 14 , 18 ]. Long-term exposure to Cd has been associated with various conditions, including various renal syndromes, osteoporosis and osteomalacia, CVD, and different types of cancer [ 14 , 15 , 19 , 20 , 21 , 22 , 23 , 24 , 25 ]. Its endocrine-disrupting properties have also been shown, suggesting its possible effects on estrogenic activity [ 26 , 27 , 28 , 29 ], alterations in semen and the testis [ 30 , 31 , 32 ], and a role in thyroid disorders [ 33 , 34 , 35 ].…”

Section: Introductionmentioning

confidence: 99%

Emerging Links between Cadmium Exposure and Insulin Resistance: Human, Animal, and Cell Study Data

Buha

Đukić-Ćosić

Ćurčić

et al. 2020

Toxics

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Recent research has helped clarify the role of cadmium (Cd) in various pathological states. We have demonstrated Cd involvement in pancreatic cancer, as well as the bioaccumulation of Cd in the pancreas. Bioaccumulation and increased toxicity suggest that Cd may also be involved in other pancreas-mediated diseases, like diabetes. Cd falls into the category of “hyperglycemic” metals, i.e., metals that increase blood glucose levels, which could be due to increased gluconeogenesis, damage to β-cells leading to reduced insulin production, or insulin resistance at target tissue resulting in a lack of glucose uptake. This review addresses the current evidence for the role of Cd, leading to insulin resistance from human, animal, and in vitro studies. Available data have shown that Cd may affect normal insulin function through multiple pathways. There is evidence that Cd exposure results in the perturbation of the enzymes and modulatory proteins involved in insulin signal transduction at the target tissue and mutations of the insulin receptor. Cd, through well-described mechanisms of oxidative stress, inflammation, and mitochondrial damage, may also alter insulin production in β-cells. More work is necessary to elucidate the mechanisms associated with Cd-mediated insulin resistance.

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Bone mineral health is sensitively related to environmental cadmium exposure- experimental and human data

Cited by 67 publications

References 57 publications

An assessment of sensitivity biomarkers for urinary cadmium burden

An assessment of sensitivity biomarkers for urinary cadmium burden

A Review on Coordination Properties of Thiol-Containing Chelating Agents Towards Mercury, Cadmium, and Lead

Emerging Links between Cadmium Exposure and Insulin Resistance: Human, Animal, and Cell Study Data

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