Abstract
Summary
Hepatic mitochondrial functional activities, as determined by ADP/O, respiratory control ratio, and phosphorylation rate with glutamate as substrate, were augmented in male Fischer rats between 22-32 weeks following ingestion of the carcinogen, 2-N-fluorenylacetamide (2-FAA). Histologically, the livers from the carcinogen-fed group all contained hyperplastic nodules characteristic of areas of regeneration; and hepatomas were found in one animal in each of the three periods studied. Previously, increased mitochondrial activities of this type were reported for animals treated with the hepatotoxins, hydrazine and ethanol, as well as during regeneration following partial hepatectomy. This stage of hepatocarcinogenesis following the long-term feeding of 2-FAA represents an additional instance wherein these mitochondrial functional activities were elevated coincident with significant liver damage. In this case, enhanced mitochondrial activities might be an expression of the presence of the hyperplastic nodules. Whether these increases were part of the pathological chain of events during carcinogenesis or exposed a phenomenon common to both carcinogenesis and regeneration could not be ascertained from these experiments.
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