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- W1999180950 abstract "It is well known that cadmium chloride administered as single, subcutaneous, sub-toxic doses selectively damages the rat testis, producing irreversible injury of the germinal epithelium and temporary damage to the interstitial tissue. Studies reported here demonstrate that: (1) this injury represents an ischemic necrosis secondary to rapid production of intertubular edema (4 to 6 hours), increased intratesticular pressure, with or without associated hemorrhage, and ultimate interference with testicular blood supply and drainage – not unlike injury following testicular artery ligation; (2) as dosage is progressively reduced to approximately one-sixth that employed by most investigators, interstitial tissue is unaffected and ischemic necrosis is supplanted by a non-necrotic degeneration of the germinal epithelium closely resembling, in its histopathology and irreparability, that occurring after vitamin E deficiency; (3) oral administration of vitamin E has no protective effect, and testes of rats critically depleted of E show no increased susceptiblity to cadmium. Observations on the nature and distribution of tubular injury, and on the vasculature of the testis and epididymis, suggest that the unusual sensitivity of the testis to cadmium is related to unique features of its vasculature; namely, the pulseless, semistagnant flow of blood in the intratesticular course of the testicular artery, which permits cadmium to alter capillary endothelium permeability, causing edema and pressure effects leading to acute anoxia at higher levels of dosage, and diminishing degrees of anoxia with decreasing dosage levels. Comparable morphological features of the proximal segment of the caput epididymis make it likewise susceptible to cadmium injury." @default.
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- W1999180950 date "1964-05-01" @default.
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- W1999180950 title "Cadmium-induced injury of the rat testis" @default.
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- W1999180950 doi "https://doi.org/10.1002/ar.1091490112" @default.
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