Revival: Biological Effects of Low Level Exposures to Chemical and Radiation (1992)

BIPHASIC DOSE-RESPONSE RELATIONSHIPS 67

Figure 4.3. Structure of 1,1,2-trichloroethylene, bromobenzene, bromoform, and
dibromodichloromethane. Toxicity of these chemicals is not potentiated by
prior dietary exposure to 10 ppm chlordecone.

Recent studies have also shown a significant activation of phosphorylase a,
a finding commensurate with the precipitous depletion of glycogen89’90 109115
and ATP.89 90115 Based on several lines of experimental evidence, a hypothe­
sis was proposed for the mechanism of the interactive toxicity of chlorde­
cone and CC14.16

Stimulation of Tissue Repair as a Hormetic Response
to Tissue Injury

First, it became necessary to hypothesize the mechanism for why an
ordinarily nontoxic dose of CC1 4 is nontoxic.55 Figure 4.4 illustrates the
mechanism of recovery from the limited liver injury observed after the

Table 4.3. Specificity of Potentiation of Halomethane Toxicity by Chlordecone

Compound Potentiation? References

CHCI3 yes 100,102
CCI4 yes 55,98,99
CBrCI3 yes 91,92
CHBr3 no 55
CBr4 no 55
CCI2CHCI no 104
Bromobenzene no 104