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Results for “BENZENE HEXACHLORIDE”

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PubMedDate not supplied

Evaluation of daily dietary intake of dichloro-diphenyl-trichloroethane (DDT) and benzene hexachloride (BHC) in India.

Duplicate samples of the diet of vegetarian adults were analyzed to estimate the residues of dichloro-diphenyl-trichloroethane (DDT) and benzene hexachloride (BHC). The total food consumed by an adult per day was collected and categorized as fatty food, non-fatty food, water, and beverages. Fatty food was the main source of these chlorinated insecticides, and it contributed almost 50% of the total dietary intake. The average total DDT and BHC consumed by an adult were 19.24 micrograms/d and 77.15 micrograms/d, respectively. Blood DDT and BHC levels reflected intake (r = 0.685 for DDT; r = 0.515 for BHC).

Adult↗

PubMed1977

Mutagenic and lethal effects of alpha-benzene hexachloride, dibutyl phthalate and trichloroethylene in Saccharomyces cerevisiae.

Saccharomyces cerevisiae strain XV185-14C for reversion studies was used to investigate the genetic activity of alpha-benzene hexachloride dibutyl phthalate and trichloroethylene. The results indicate that none of the three compounds was genetically active when yeast cells were treated in phosphate buffer (pH 7.0) in the absence of metabolic conversion. However, in the presence of the 9000 g supernatant of mice liver homogenate, NADP, glucose-6-phosphate, phosphate buffer (PH 7.4), MgCl2, KCl, the components which were used for the metabolic conversion, trichloroethylene porved to be a powerful mutagen. It increases the frequency of homoserine, histidine and lysine revertants over those of the control levels. Trichloroethylene appears to induce frameshift as well as base substitution mutations.

Animals↗

PubMed1989

Genotoxic effect of benzene hexachloride in cultured human lymphocytes.

Chromosomal aberrations, sister chromatid exchanges, mitotic index and cell kinetics were observed in human peripheral lymphocytes after treatment with four different concentrations (0.0125, 0.025, 0.05 and 0.1 microgram/ml) of benzene hexachloride (BHC), an organochlorine pesticide. Cells were treated with BHC for 24, 48 and 72 h. There was a dose-dependent increase in the frequency of chromosomal aberrations and sister chromatid exchanges. A significant decrease in mitotic index was observed at all concentrations and times of exposure. BHC did not show a significant effect on cell kinetics.

Adult↗

PubMed1990

Trends of PCB, hexachlorobenzene, and beta-benzene hexachloride levels in the adipose tissue of the U.S. population.

Results are presented on the levels of selected toxic chemicals in the adipose tissue of the U.S. population. Estimates of baseline levels and time trends are presented for the chemicals beta-benzene hexachloride (beta-BHC), hexachlorobenzene, and polychlorinated biphenyls (PCBs). The statistical analyses are based on chemical data obtained from analysis of tissue specimens collected from a nationally representative sample of autopsied cadavers and surgical patients by EPA's National Human Adipose Tissue Survey during the period 1970 through 1983. The results show that while nearly the entire U.S. population has detectable levels of these chemicals, the actual concentration levels of beta-BHC and PCBs are steadily decreasing and the levels of HCB are remaining fairly constant. Comparisons of levels across demographic subpopulations show that there are some differences in concentration levels across geographic regions, age groups, and race groups.

Adipose Tissue↗

PubMed2005

Alpha-benzene hexachloride exerts hormesis in preneoplastic lesion formation of rat hepatocarcinogenesis with the possible role for hepatic detoxifying enzymes.

Recently there has been a shift in the prevailing paradigm regarding the dose dependence of carcinogen action with increasing acceptance of hormesis phenomenon, although underlying mechanisms remain to be established. To ascertain whether alpha-benzene hexachloride (alpha-BHC) might act by hormesis, rats were initiated with diethylnitrosamine and then alpha-BHC ranging from 0.01 to 500 ppm was administered in the diet for 10 weeks. The highest concentration of alpha-BHC significantly increased the number and area of glutathione S-transferase placental form (GST-P) positive foci, preneoplastic lesions in the liver, but its low dose, 0.05 ppm, caused significant reduction, showing a J-shape dose-response curve. The proliferating cell nuclear antigen positive index for GST-P positive foci in the low dose-treated group was significantly reduced. The dose response curves of CYP450 content, NADPH-P450 reductase activity and 8-hydroxydeoxyguanosine formation revealed the same pattern as GST-P positive foci data. The response curves of CYP2B1 and 3A2 in their activities, protein and mRNA expression showed a threshold but CYP2C11 activity exhibited an inverted J-shape. These results might suggest the possibility of hormesis of alpha-BHC at early stages of rat hepatocarcinogenesis. The possible mechanism involves induction of detoxifying enzymes at low dose, influencing free radical production and oxidative stress, and consequently pathological change in the liver.

8-Hydroxy-2'-Deoxyguanosine↗

PubMed1955