Effect of Cadmium Salts on Testicular Tissue

Parízek, J; Zahor, Z

doi:10.1038/1771036b0

Cited by 194 publications

(57 citation statements)

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“…In about the mid-1950s Parizek (1957) rediscovered and exhaustively investigated the destructive effect of Cd on testicular tissue. The sterilizing effect of Cd is rapid and experimental animals may become permanently sterile in as short duration as 24hrs post administration (Parizek and Zahor, 1956;Parizek, 1957). The testes thus seem to be extremely sensitive to the toxic effects of Cd; hemorrhagic necrosis of rodent testes can be induced by Cd concentrations as low as 0.15ug/g (Parizek, 1957).…”

Section: Discussionmentioning

confidence: 99%

High cadmium / zinc ratio in cigarette smokers: potential implications as a biomarker of risk of prostate cancer.

Anetor

Ajose²,

Anetor³

et al. 2010

Nig. J. Phys Sci

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SummaryTobacco smoke may be one of the most common sources of cadmium (Cd) in the general population, particularly in the rising population of smokers in developing countries. Although a relationship between both cigarette smoking and environmental Cd contamination with prostate cancer exist, the mechanisms are unclear. Most prospective cohort studies found a positive association between current smoking and a fatal cancer of the prostate. We investigated the interaction between zinc and cadmium and the potential risk of prostate cancer in smokers. Serum cadmium level was significantly (P<0.001) higher in smokers compared with non-smokers, the level in smokers was three-fold that in non-smokers. In contrast zinc was significantly (P<0.001) reduced in smokers compared with non-smokers. Unlike Zn, Cu was significantly (P<0.05) higher in smokers than in nonsmokers. Iron (Fe) though higher in smokers was not significantly different. Zinc: cadmium ratio was very significantly (P<0.001) reduced, implying high cadmium: zinc ratio. This ratio was 4.5-fold the level in nonsmokers. Total protein, albumin and total globulin levels were all significantly (P<0.001) reduced in smokers compared with non-smokers respectively. Potassium (K + ) was significantly (P<0.05) higher in smokers than in non-smokers. Magnesium (Mg) was significantly (p<0.01) reduced in smokers compared to non-smokers. Altered Zn status culminating in high Cd:Zn ratio appears the central factor in smokers; leading to oxidative stress, DNA damage, mutation, impaired DNA repair, P 53 expression, angiogenic effect of Cu and impaired vitamin A metabolism. These converge in the risk of the carcinogenic process, suggesting high Cd: Zn ratio as the critical determinant of the risk of prostate cancer in smokers and possibly a biomarker of susceptibility to this environmental disease.

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Section: Discussionmentioning

confidence: 99%

High cadmium / zinc ratio in cigarette smokers: potential implications as a biomarker of risk of prostate cancer.

Anetor

Ajose²,

Anetor³

et al. 2010

Nig. J. Phys Sci

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“…The testes are another target affected adversely by Cd 2+ (Gunn et al, 1963a(Gunn et al, , 1963bKar and Das, 1960;Parizek, 1957;Parizek and Zahor, 1956). Acute testicular necrosis and the destruction of the seminiferous tubules have been shown to occur in rats and mice after a single injection of Cd 2+ .…”

Section: Mimicry Of CD 2+ In Testismentioning

confidence: 99%

Molecular and ionic mimicry and the transport of toxic metals

Bridges

Zalups

2005

Toxicology and Applied Pharmacology

677

460

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Despite many scientific advances, human exposure to, and intoxication by, toxic metal species continues to occur. Surprisingly, little is understood about the mechanisms by which certain metals and metal-containing species gain entry into target cells. Since there do not appear to be transporters designed specifically for the entry of most toxic metal species into mammalian cells, it has been postulated that some of these metals gain entry into target cells, through the mechanisms of ionic and/or molecular mimicry, at the site of transporters of essential elements and/or molecules. The primary purpose of this review is to discuss the transport of selective toxic metals in target organs and provide evidence supporting a role of ionic and/or molecular mimicry. In the context of this review, molecular mimicry refers to the ability of a metal ion to bond to an endogenous organic molecule to form an organic metal species that acts as a functional or structural mimic of essential molecules at the sites of transporters of those molecules. Ionic mimicry refers to the ability of a cationic form of a toxic metal to mimic an essential element or cationic species of an element at the site of a transporter of that element. Molecular and ionic mimics can also be sub-classified as structural or functional mimics. This review will present the established and putative roles of molecular and ionic mimicry in the transport of mercury, cadmium, lead, arsenic, selenium, and selected oxyanions in target organs and tissues.

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“…It is known that Cd-induced testicular necrosis is common across all animal species having testes: rodents, opossum, armadillos, frogs, pigeons, roosters, and fish (12)(13)(14)(15)(16)(17). Cellular events that precede Cd-induced testicular toxicity indicate that vascular endothelial cell injury is the earliest and, perhaps, the causative event (16,(18)(19)(20)(21)(22)(23)(24).…”

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confidence: 99%

Identification of mouse SLC39A8 as the transporter responsible for cadmium-induced toxicity in the testis

Dalton

Wang

et al. 2005

Proc. Natl. Acad. Sci. U.S.A.

267

234

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Testicular necrosis is a sensitive endpoint for cadmium (Cd 2؉ , Cd) toxicity across all species tested. Resistance to Cd-induced testicular damage is a recessive trait assigned to the Cdm locus on mouse chromosome 3. We first narrowed the Cdm-gene-containing region to 880 kb. SNP analysis of this region from two sensitive and two resistant inbred strains demonstrated a 400-kb haplotype block consistent with the Cd-induced toxicity phenotype; in this region is the Slc39a8 gene encoding a member of the solute-carrier superfamily. Slc39a8 encodes SLC39A8 (ZIP8), whose homologs in plant and yeast are putative zinc transporters. We show here that ZRT-, IRT-like protein (ZIP)8 expression in cultured mouse fetal fibroblasts leads to a >10-fold increase in the rate of intracellular Cd influx and accumulation and 30-fold increase in sensitivity to Cd-induced cell death. The complete ZIP8 mRNA and intron-exon splice junctions have no nucleotide differences between two sensitive and two resistant strains of mice; by using situ hybridization, we found that ZIP8 mRNA is prominent in the vascular endothelial cells of the testis of the sensitive strains of mice but absent in these cells of resistant strains. Slc39a8 is therefore the Cdm gene, defining sensitivity to Cd toxicity specifically in vascular endothelial cells of the testis. metal influx ͉ vascular endothelial cells ͉ solute carrier gene superfamily ͉ in situ hybridization C d is a toxic and carcinogenic nonessential metal (1), which can enter the body through the intestine, skin, and lung and accumulates in the kidney (1-3). The level of Cd in the environment has risen with advances in industrialization, and the role of Cd in human disease is of increasing concern. The mechanisms of Cd toxicity are poorly understood, although it is known that Cd exerts its effects intracellularly, and there are polypeptides such as metallothionein (4) and reduced glutathione (5) that bind Cd and afford protection. The subcellular events by which Cd is taken up by cells or removed from cells remain obscure, although such knowledge could provide potential therapeutic targets for protection or intervention against Cd toxicity. Several proteins transport Cd into bacteria, yeast, plants, and mammalian cells in culture (6-11), but their specific roles in causing toxicity are unclear; these studies underscore the difficulties in extrapolating from observations in cell culture to the intact animal.Nature has provided a fascinating genetic system as a foothold into identifying a gene involved in Cd toxicity. It is known that Cd-induced testicular necrosis is common across all animal species having testes: rodents, opossum, armadillos, frogs, pigeons, roosters, and fish (12-17). Cellular events that precede Cd-induced testicular toxicity indicate that vascular endothelial cell injury is the earliest and, perhaps, the causative event (16,(18)(19)(20)(21)(22)(23)(24).Some inbred mouse strains are resistant to Cd-induced testicular toxicity (25). The resistance phenotype segregates largely as a...

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Effect of Cadmium Salts on Testicular Tissue

Cited by 194 publications

References 1 publication

High cadmium / zinc ratio in cigarette smokers: potential implications as a biomarker of risk of prostate cancer.

High cadmium / zinc ratio in cigarette smokers: potential implications as a biomarker of risk of prostate cancer.

Molecular and ionic mimicry and the transport of toxic metals

Identification of mouse SLC39A8 as the transporter responsible for cadmium-induced toxicity in the testis

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