Hepatic Mitochondrial Alteration in CD-1 Mice Associated with Prenatal Exposures to Low Doses of Perfluorooctanoic Acid (PFOA)

Spermatogonial stem-cell survival after irradiation injury has been studied in rodents by histological counts of surviving cells. Many studies, including previous work from our laboratory, show that the spermatogonial population demonstrates a heterogeneous response to irradiation. The spermatogonia increase in radio-sensitivity as differentiation proceeds through the sequence As - Apr - A1 - A2 - A3 - A4 - In - B. The stem (As) cell is the most resistant and the B cell is the most sensitive. The purpose of this work is to investigate the response of spermatogonial cell to low doses (less than 10 0 rads) of helium particle irradiation.

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Mitochondrial Changes in Cholestasis

Proceedings, annual meeting, Electron Microscopy Society of America ◽

10.1017/s0424820100094553 ◽

1972 ◽

Vol 30 ◽

pp. 258-259

Author(s):

F. G. Zaki

Keyword(s):

Biliary Obstruction ◽

Alcoholic Cirrhosis ◽

Ultrastructural Changes ◽

List Type ◽

Common Occurrence ◽

Extrahepatic Cholestasis ◽

Mitochondrial Alteration ◽

Extrahepatic Biliary Obstruction ◽

Liver Biopsies ◽

Mitochondrial Anomalies

Alterations of liver cell mitochondria represent pathologic phenomenon of a fundamental nature. Mitochondrial anomalies have been often described in association with cholestasis. In attempt to determine whether a given pattern of mitochondrial alteration has any correlation with the cause of cholestasis, liver biopsies were examined from 38 patients showing :a. extrahepatic cholestasis due to complete or partial extrahepatic biliary obstruction (8 cases proven at operation)b. intrahepatic cholestasis due to drugs (9 cases), viral hepatitis (6 cases) and alcoholic cirrhosis (15 cases).Mitochondria exhibiting ultrastructural changes due to aging or to the ‘wear and teart’ processes were not considered. In this study, the only profound and most prominent mitochondrial deformation was reported on basis of their common occurrence in randomly examined sections.

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Potentiation of bromotrichloromethane hepatotoxicity in male rats exposed to 10 ppm dietary chlordecone: Electron Microscopic and biochemical study

Proceedings, annual meeting, Electron Microscopy Society of America ◽

10.1017/s0424820100158972 ◽

1990 ◽

Vol 48 (3) ◽

pp. 284-285

Author(s):

O. M. Faroon ◽

R. W. Henry ◽

M. G. Soni ◽

H. M. Mehendale

Keyword(s):

Free Radical ◽

Biochemical Study ◽

Prior Exposure ◽

Male Rats ◽

Cellular Injury ◽

Low Doses ◽

Mixed Function Oxidase ◽

Electron Microscopic ◽

Potent Inducer ◽

Cellular Energy

Previous work has shown that mirex undergoes photolytic dechlorination to chlordecone (CD) (KeponeR) in the environment. Much work has shown that prior exposure to nontoxic levels of CD causes potentiation of hepatotoxicity and lethality of CCl4, BrCCl3 and other halomethane compounds. Potentiation of bromotrichloromethane hepatotoxicity has been associated with compounds that stimulate the activity of hepatic mixed-function oxidase (MFO). An increase in the metabolism of halomethane by the MFO to a free radical initiates peroxidative decomposition of membranal lipids ending in massive cellular injury. However, not all MFO inducers potentiate BrCCl3 hepatotoxicity. Potentiation by much larger doses of phenobarbital is minimal and th at by a more potent inducer of MFO, mirex, is negligible at low doses. We suggest that the CD and bromotrichloromethane interaction results in a depletion of cellular energy and thereby reducing the cellular ability to undergo mitosis.

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