Cytopathological Changes Induced by Cadmium-Exposure in Canine Proximal Tubular Cells: A Cytochemical and Ultrastructural Study

Hamada, Tetsuo; Tanimoto, Akihide; Iwai, Shigetoshi; Fujiwara, Hitoshi; Sasaguri, Yasuyuki

doi:10.1159/000188227

Cited by 36 publications

(25 citation statements)

References 19 publications

(21 reference statements)

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“…Although our findings provide no direct insight regarding the mechanism of cadmium induction of germ cell apoptosis, Betka and Callard (1999) have found that, although cytosolic cadmium-binding components other than heavy-metal-binding metallothionein can, to some extent, account for the cadmium accumulation gradient in the shark testis, a second nuclear-associated component of cadmium is present in larger amounts in immature than in mature spermatogonial regions in the testis of Squalus. Cadmium has a high affinity for nucleic acids and accumulates within the nuclear compartment, even when present in trace amounts (Snow 1992;Hamada et al 1994). Nuclear-associated cadmium may displace zinc in polymerases, other metalloenzymes or transcription factors, all of which are present in larger amounts in the nuclei of proliferating cells (Din and Frazier 1985) or it may directly induce chromatin changes (Banfalvi et al 2005).…”

Section: Discussionmentioning

confidence: 99%

Stage-dependency of apoptosis and the blood-testis barrier in the dogfish shark (Squalus acanthias): cadmium-induced changes as assessed by vital fluorescence techniques

McClusky

2006

Cell Tissue Res

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Naturally occurring heavy metals and synthetic compounds are potentially harmful for testicular function but evidence linking heavy metal exposure to reduced semen parameters is inconclusive. Elucidation of the exact stage at which the toxicant interferes with spermatogenesis is difficult because the various germ cell stages may have different sensitivities to any given toxicant, germ cell development is influenced by supporting testicular somatic cells and the presence of inter-Sertoli cell tight junctions create a blood-testis barrier, sequestering meiotic and postmeiotic germ cells in a special microenvironment. Sharks such as Squalus acanthias provide a suitable model for studying aspects of vertebrate spermatogenosis because of their unique features: spermatogenesis takes place within spermatocysts and relies mainly on Sertoli cells for somatic cell support; spermatocysts are linearly arranged in a maturational order across the diameter of the elongated testis; spermatocysts containing germ cells at different stages of development are topographically separated, resulting in visible zonation in testicular cross sections. We have used the vital dye acridine orange and a novel fluorescence staining technique to study this model to determine (1) the efficacy of these methods in assays of apoptosis and blood-testis barrier function, (2) the sensitivity of the various spermatogonial generations in Squalus to cadmium (as an illustrative spermatotoxicant) and (3) the way that cadmium might affect more mature spermatogenic stages and other physiological processes in the testis. Our results show that cadmium targets early spermatogenic stages, where it specifically activates a cell death program in susceptible (mature) spermatogonial clones, and negatively affects blood-testis barrier function. Since other parameters are relatively unaffected by cadmium, the effects of this toxicant on apoptosis are presumably process-specific and not attributable to general toxicity.

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Section: Discussionmentioning

confidence: 99%

Stage-dependency of apoptosis and the blood-testis barrier in the dogfish shark (Squalus acanthias): cadmium-induced changes as assessed by vital fluorescence techniques

McClusky

2006

Cell Tissue Res

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“…Cadmium may lead to interstitial fibrosis and apoptosis in proximal tubule cells following tubular cell necrosis and inflammation [49,50] . In the kidney, cytosolic cadmium gives rise to the formation of free oxygen radicals.…”

Section: Discussionmentioning

confidence: 99%

The Effects of Chronic Cadmium Toxicity on the Hemostatic System

Koçak

Akçıl²

2006

Pathophysiol Haemos Thromb

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Cadmium, a highly toxic heavy metal, is distributed widely in the general environment. The characteristic clinical manifestations of chronic cadmium intoxication include renal proximal tubular dysfunction, osteomalacia and anemia. Accumulating evidence suggests that cadmium toxicity may also affect various organs such as the liver, lung, testis and hematopoietic system. The aim of this study was to determine the effect of chronic cadmium exposure on the anticoagulant system in rats. Fourty-five adult Wistar albino rats were randomly allocated into 2 groups. While the control group was given tap water, the animals in the cadmium group were treated with 15 ppm CdCl₂ for 4 weeks. Blood cadmium concentration, prothrombin time, activated partial thromboplastin time, plasma protein C and antithrombin activity, and platelet count were determined in the rats. Blood cadmium concentrations increased in the experiment group compared to the control group (p < 0.001). Results also show that cadmium exposure shortened prothrombin time (p < 0.05) and activated partial thromboplastin time (p < 0.01) in rats. Protein C (p < 0.001) and antithrombin (p < 0.001) decreased to statistically significantly lower levels in rat plasma after cadmium exposure when compared to the control group. When the number of thrombocytes was compared between 2 groups, a decrease was observed in the group treated with CdCl₂, which was, however, not statistically significant (p > 0.05). In conclusion, when the parameters of the hemolytic system are considered, the decrease in protein C and antithrombin activities and the shortening of prothrombin time and activated partial thromboplastin time suggests the presence of a hypercoagulable state during chronic cadmium intoxication. Therefore, it may be stated that chronic cadmium toxicity sets the stage for hypercoagulation and hence increases the risk of thrombosis.

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“…5). Cadmium can induce apoptosis in isolated T lymphocytes (11) and cultured LLC-PK1 cells (31) and lead to apoptotic cell damage in canine proximal tubules (17) and rat testicular tissue (56). Most observations of Cd 2ϩ -mediated cell death are consistent with the caspase-dependent intrinsic pathway of apoptosis.…”

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confidence: 84%

Cadmium inhibits both intrinsic and extrinsic apoptotic pathways in renal mesangial cells

Gunawardana

Martinez²,

Wu³

et al. 2006

American Journal of Physiology-Renal Physiology

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Cytopathological Changes Induced by Cadmium-Exposure in Canine Proximal Tubular Cells: A Cytochemical and Ultrastructural Study

Cited by 36 publications

References 19 publications

Stage-dependency of apoptosis and the blood-testis barrier in the dogfish shark (Squalus acanthias): cadmium-induced changes as assessed by vital fluorescence techniques

Stage-dependency of apoptosis and the blood-testis barrier in the dogfish shark (Squalus acanthias): cadmium-induced changes as assessed by vital fluorescence techniques

The Effects of Chronic Cadmium Toxicity on the Hemostatic System

Cadmium inhibits both intrinsic and extrinsic apoptotic pathways in renal mesangial cells

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