Cadmium — A metallohormone?

Byrne, Celia; Divekar, Shailaja D.; Storchan, Geoffrey B.; Parodi, Daniela A.; Martin, Mary Beth

doi:10.1016/j.taap.2009.03.025

Cited by 157 publications

(121 citation statements)

References 81 publications

(86 reference statements)

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“…Consistent with these results is the hypothesized role of cadmium as a metallohormone [Byrne et al 2009]. Once cadmium enters cells the damage it induces has been attributed primarily to its interference with zincmediated metabolic processes, possibly by molecular mimicry of zinc [Bridges and Zalups 2005].…”

Section: Animal and In Vitro Studiesmentioning

confidence: 61%

Adverse Effects of Low Level Heavy Metal Exposure on Male Reproductive Function

Wirth

Mijal

2010

Systems Biology in Reproductive Medicine

242

164

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Lead, cadmium, mercury, and arsenic, often referred to as ''heavy metals'', are toxic for wildlife, experimental animals, and humans. While experimental animal and human occupational studies with high exposure levels generally support an adverse role for these metals in human reproductive outcomes, information on the effects of low, environmentally-realistic exposure levels of these metals on male reproductive outcomes is limited. We review the literature on effects of exposure to low levels of these metals on measures of male fertility (semen quality and reproductive hormone levels) and provide supporting evidence from experimental and occupational studies. Potentially modifying effects of genetic polymorphisms on these associations are discussed. A brief review of the literature on the effects of three trace metals, copper, manganese, and molybdenum, that are required for human health, yet may also cause adverse reproductive effects, follows. Overall, there were few studies examining the effects of exposure to low levels of these metals on male reproductive health. For all metals, there were several well-designed studies with sufficient populations appropriately adjusted for potential confounders and many of these reported harmful effects. However, many studies lacked sufficient numbers of participants to be able to detect differences in outcomes between exposed and non-exposed individuals, did not clearly identify the source and characteristics of the participants, and did not control for other exposures that could alter or contribute to the outcomes. The evidence for the effects of low exposure was strongest for cadmium, lead, and mercury and less certain for arsenic. The potential modifying effects of genetic polymorphisms has not been fully explored. Additional studies on the reproductive effects of these toxic ubiquitous metals on male reproduction are required to expand the knowledge base and to resolve inconsistencies.

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Section: Animal and In Vitro Studiesmentioning

confidence: 61%

Adverse Effects of Low Level Heavy Metal Exposure on Male Reproductive Function

Wirth

Mijal

2010

Systems Biology in Reproductive Medicine

242

164

View full text Add to dashboard Cite

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“…In addition, in Drosophila cells, depletion of hsc70 has been proven to lead to upregulation of hsp27 [23], and therefore the two events could be linked in PLP2 asODN-transfected cells. On the other hand, it is known that hsp27 promoter contains an imperfect but functional estrogen-responsive element and that Cd is a metallo-estrogen, since it binds and activates steroid receptors [24,25]; therefore, PLP2 might be involved in the counteraction of such activating role played by Cd on hsp27 gene. Furthermore, Kindas-Mügge et al [26] demonstrated the decrease of the proliferation rate of hsp27-overexpressing MDA-MB231 cells; thus, it can be hypothesized that PLP2-induced restraining effect on hsp27 expression may be addressed to protect cell growth behavior from the toxic effect of the metal.…”

Section: Discussionmentioning

confidence: 99%

Effect of transfection with PLP2 antisense oligonucleotides on gene expression of cadmium-treated MDA-MB231 breast cancer cells

2012

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“…Cadmium can also act as an endocrine disruptor, and it is carcinogenic. (Järup et al, 1998;Waalkes, 2003; for reviews, see Agency for Toxic Substances & Disease Registry, Toxicological Profile for Cadmium, 2008, http:// www.atsdr.cdc.gov/toxprofiles/tp.asp?idϭ48 &tidϭ15; Byrne et al, 2009;Joseph, 2009).…”

mentioning

confidence: 99%

Mechanisms of Cadmium-Induced Proximal Tubule Injury: New Insights with Implications for Biomonitoring and Therapeutic Interventions

Prozialeck

Edwards

2012

J Pharmacol Exp Ther

214

150

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Cadmium is an important industrial agent and environmental pollutant that is a major cause of kidney disease. With chronic exposure, cadmium accumulates in the epithelial cells of the proximal tubule, resulting in a generalized reabsorptive dysfunction characterized by polyuria and low-molecular-weight proteinuria. The traditional view has been that as cadmium accumulates in proximal tubule cells, it produces a variety of relatively nonspecific toxic effects that result in the death of renal epithelial cells through necrotic or apoptotic mechanisms. However, a growing volume of evidence suggests that rather than merely being a consequence of cell death, the early stages of cadmium-induced proximal tubule injury may involve much more specific changes in cell-cell adhesion, cellular signaling pathways, and autophagic responses that occur well before the onset of necrosis or apoptosis. In this commentary, we summarize these recent findings, and we offer our own perspectives as to how they relate to the toxic actions of cadmium in the kidney. In addition, we highlight recent findings, suggesting that it may be possible to detect the early stages of cadmium toxicity through the use of improved biomarkers. Finally, some of the therapeutic implications of these findings will be considered. Because cadmium is, in many respects, a model cumulative nephrotoxicant, these insights may have broader implications regarding the general mechanisms through which a variety of drugs and toxic chemicals damage the kidney.

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Cadmium — A metallohormone?

Cited by 157 publications

References 81 publications

Adverse Effects of Low Level Heavy Metal Exposure on Male Reproductive Function

Adverse Effects of Low Level Heavy Metal Exposure on Male Reproductive Function

Effect of transfection with PLP2 antisense oligonucleotides on gene expression of cadmium-treated MDA-MB231 breast cancer cells

Mechanisms of Cadmium-Induced Proximal Tubule Injury: New Insights with Implications for Biomonitoring and Therapeutic Interventions

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