Fate and specific tissue retention of toxaphene in mice

Abstract

Series of female virgin and pregnant albino mice were i.v. injected with 14C-labelled- or unlabelled toxaphene (16 mg/kg b.w.). After survival times ranging from 1 min to 32 days the toxaphene distribution in the body was studied using whole-body autoradiography and capillary gas-chromatography. Autoradiographic studies have shown that after an initial accumulation in the liver, brown fat, lung, brain, kidney, and ovaria (corpora lutea) there was a gradual redistribution of radioactivity to the white fat within 4 h postinjection. The labelling was then decreasing rapidly and only negligible amounts of the radioactivity were present in the adipose tissue after 32 days. In the fetus only the liver and adrenals showed a distinct labelling. A specific and persistent accumulation of the label was detected in some zones of the adrenal cortex suggesting a possible direct interference of toxaphene with adrenal steroid hormone synthesis. The gas chromatographic pattern of toxaphene-derived residues in the tissue samples resembled that of the technical toxaphene, but was changing in different tissues with the time. The liver chromatograms indicated more extensive formation of metabolites.

Tissue accumulation of lipoprotein associated toxaphene in normo- and hypolipidemic mice

“…The redistribution of radioactivity into adipose tissue observed in the present investigation 4 h after injection of the different toxaphene preparations to the normolipidemic mice is comparable to results from earlier distribution studies of toxaphene and other persistent chlorinated hydrocarbons (B~ickstr6m et al 1965;Brandt 1977;Brandt et al 1980;Mohammed et al 1983). This redistribution of label conceivably results from the association of the more lipophilic congeners of toxaphene retained in the liver with the endogenous lipoproteins and subsequent transport via the circulatory system.…”

“…This redistribution of label conceivably results from the association of the more lipophilic congeners of toxaphene retained in the liver with the endogenous lipoproteins and subsequent transport via the circulatory system. In this way the parent agent and/or its congeners would become available for uptake into adipose tissues (see also Mohammed et al 1983;Lutz and Dedrick 1987). Another factor involved in the delayed accumulation in the fat of 14C-toxaphene and other lipophilic xenobiotics, e.g.…”

“…Toxaphene has been shown to be rapidly removed from the blood and distributed to the different tissues of mice after intravenous injection (Mohammed et al 1983). In rat plasma, toxaphene is mainly associated with the HDL fraction and the Abbreviations: VLDL = very low density lipoproteins (d < 1.006 g/ml); LDL = low density lipoproteins (d= 1.020-1.060 g/ml); HDL = high density lipoproteins (d = 1.070-1.21 g/ml); DMSO = dimethyl sulfoxide; 4 APP = 4-aminopyrazolo (3,4-d) pyrimidine; US EPA = US Environmental Protection Agency Offprint requests to: A. Mohammed protein rich bottom fraction, respectively (Mohammed unpublished observations).…”

Distribution of toxaphene, DDT, and PCB among lipoprotein fractions in rat and human plasma

“…Although its fate in the organism has been studied (Crowder and Dindal 1974;Ohsawa et al 1975;Saleh et al 1979;Pollock and Kilgore 1980;Mohammed et al 1983), no data seem to be available on the interaction between toxaphene and macromolecules present in plasma. In view of recent findings concerning the interference of the substance with the synthesis and/or release of adrenal corticosteroids in rats (Mohammed et al 1985), it was of interest to look for possible interference of toxaphene with the metabolism of plasma lipids.…”

Toxaphene [MAK Value Documentation, 2003]

“…16 days after the injection only traces of radioactivity were found, the highest level in abdominal adipose tissue. After 32 days, radioactivity was no longer detectable (Mohammed et al 1983).…”