Effects of sub‐chronic low‐level dietary intake of chlordane on rats with cirrhosis of the liver.

Abstract

Male rats, 60 days old, were treated with chlordane during or after induction of liver cirrhosis with carbon tetrachloride to determine the effect of treatment with chlordane on the response of the rats to the disease. When liver cirrhosis was induced simultaneously with chlordane treatment the disease symptoms were aggravated; the lipid content of the tissue was lowered significantly, growth rate was significantly lower than controls and there was no apparent replacement of damaged liver tissue by liver growth. The cytochrome P450 content of the liver was similar after both treatments. Continuation of the chlordane treatment after termination of the carbon tetrachloride treatment brought about a more rapid recovery from the induced cirrhotic condition. All these responses were to a dose range one tenth the recommended "no effect" level for healthy animals.

DNA in rat hepatocyte nuclei: effects of treatment with low levels of carbon tetrachloride and (or) chlordane

“…The reverse has also been shown to occur (24). A high degree of polyploidy coupled with induction of the microsomal enzyme system in groups D and E (14) was in contrast with expected results. There was no stimulation of the microsomal system in group C (14).…”

“…In group C, and by corollary group E, after 10 weeks of exposure to CCl, there was hypertrophy of the liver, while in group D there was no such growth (14). This would be in agreement with Takata (24) if argued that the administration of CCI, and chlordane simultaneously stimulated the liver to produce functional proteins to metabolize the toxicants, at the expense of regeneration.…”

“…If the effect of chlordane and CCI, was only an increased level of induction, then the same degree of decondensation would be expected for both groups D and E as the same genes would be activated. Similarly, there was decondensation of the chromatin in group B though there was no detectable induction of the microsomal enzymes (14). The results suggest that the exposure to CCl, predisposed the cell to respond to treatment with chlordane.…”

“…This would be in agreement with Takata (24) if argued that the administration of CCI, and chlordane simultaneously stimulated the liver to produce functional proteins to metabolize the toxicants, at the expense of regeneration. When chlordane was administered after CCl, exposure (group E) the stimulation of the detoxification system (microsomal enzymes) was greater than in group D (14), but so also was the increase in the ploidy level of the hepatocytes. The high ploidy level combined with the high degree of induction would indicate that the damaged cells were stimulated to respond more readily to the presence of chlordane.…”

Wildlife Toxicity Assessment for Chlordane

“…The same study found an inverse correlation between ovary length and chlordane levels in female polar bears. The liver appears to be the primary target organ of chlordane toxicity in experimental studies [9][10][11][12]19,23,24,27,47]; other target organs include the testis [18], kidney [12], and possibly the brain [13,20]. Table 22.2 summarizes the studies that highlight the effects of chlordane.…”