Acute renal failure due to proliferative nephritis from snake bite poisoning.
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Biomedical subjects
Publications and source records attributed to J Reddy.
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Male wild-type mice (Cs(a) strain) were treated with ethyl-alpha-p-chlorophenoxyisobutyrate (CPIB), a hypolipidemic drug which enhances hepatic catalase synthesis and induces rapid and significant increase in the number of microbody (peroxisome) profiles in liver cells. Numerous microbody profiles, several of them appearing in clusters and retaining membranous continuities, were observed in liver cells of CPIB-treated mice. They showed a significant variation in size and configuration, and the presence or absence of the nucleoid or core did not appear to bear any relation to the size or shape of microbody profiles. Nucleoids were encountered frequently in microbody profiles measuring as small as 0.1 mu in diameter. Numerous continuities between two or more anucleoid and/or nucleoid-containing microbody profiles of different sizes and shapes were seen. These findings are inconsistent with the concept that the smaller peroxisomes are the possible precursors or progenitors of their larger counterparts. Detailed examination of numerous electron micrographs revealed irregular dilatations and tortuosities of the endoplasmic reticulum (ER) containing electron-opaque peroxisomal material displaying the characteristic appearance of matrix and usually containing irregular cores. Transitions of rough ER to smooth ER in which microbody proteins accumulated were also apparent. Numerous continuities between several microbody profiles and continuities between microbody profiles and ER are interpreted as accumulations of peroxisomal proteins in dilated tortuous channels of ER. These observations strongly suggest that the microbody proteins constitute a common pool, circulating constantly in the dilated ER channels. The size, shape and number of microbody profiles appear to reflect the amount of peroxisomal proteins present in the pool. These observations clearly suggest that the microbodies do not exist as individual entities.
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Male rats were given 0.25% CPIB (ethyl chlorophenoxyisobutyrate) for 4 weeks at which time their liver cells showed the typical increase in number of microbodies (peroxisomes). During the first week after withdrawal of CPIB and simultaneous injection of allylisopropylacetamide (AIA), an inhibitor of catalase synthesis, the microbody matrix, in peroxidase preparations, showed marked decrease in electron opacity. In liver cells of rats from which CPIB was withdrawn but which were not given AIA, there were interruption in the limiting membrane and almost total loss of microbody matrix within 3 days. Simultaneous with the loss of matrix content, the hepatic catalase activity decreased from an average 80 units/mg protein to less than 10 units/mg protein. In liver cells of Mastomys natalensis, a multimammate rodent, withdrawal of CPIB was associated with the frequent occurrence of bare microbody nucleoids situated free in the hyaloplasm. The ultrastructural observations and the associated decrease in catalase activity suggest that one means of disposal of microbodies is by rather rapid dissolution or leakage of their matrix enzymes into the surrounding hyaloplasm.
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