Biomedical subjects
Publications and source records attributed to M G Rozen.
Inhalation of benzene produces a prolongation of mouse red blood cell glycerol hemolysis time. This was not observed in red blood cells directly incubated in benzene. Increased resistance to the hemolytic action of glycerol should be explored as a potentially useful biological monitoring procedure in the red blood cells of benzene-exposed humans.
Groups of C57BL/6J, male mice were exposed to 300 ppm benzene via inhalation for 115 exposures (6 h/day, 5 days/week), a regimen known to cause thymic lymphoma in these animals. The effects of these exposures on lymphoid parameters were determined by measuring the numbers of B- and T-lymphocytes and mitogen-induced proliferation of B- and T-lymphocytes in bone marrow, spleen, and thymus after 6, 30, and 115 exposures. The numbers of B-lymphocytes in bone marrow and spleen and the numbers of T-lymphocytes in thymus and spleen were found to be markedly reduced after all 3 periods. Mitogen-induced proliferation of bone marrow and splenic B-lymphocytes exhibited a progressive depression throughout the exposure period reaching a point of no observable response after 115 exposures. Splenic T-cell mitogen-induced proliferation was also markedly depressed throughout the exposures, but there was no evidence of a progressive decline in this response during the exposures. Bone marrow cellularity increased 3-fold and the numbers of thymic T-cells increased 15-fold in benzene-exposed mice between the 6th and 30th exposure. No corresponding increase in splenic cells was observed in benzene-exposed mice during this interval. The marked increases in the numbers of cells in bone marrow and thymus are interpreted as arising from compensatory proliferation of a subpopulation of cells in response to the exposures. The absence of increases in cell number in the spleen is interpreted as reflecting the lack of lymphoid restorative capacity in this organ. The marked increases of thymic and bone marrow cellularity are discussed relative to the known ability of this benzene exposure regimen to produce thymic lymphoma in these animals.
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In a short-term (6 h/day X 6 days) benzene inhalation dose-response study, mitogen-induced blastogenesis of both B- and T-lymphocytes in male, C57Bl mice was observed to be significantly depressed at relatively low levels of benzene. Exposure to 10 ppm benzene resulted in a significant depression in femoral lipopolysaccharide (LPS)-induced B-colony-forming ability, while total numbers of B-lymphocytes at this concentration were not significantly depressed. Similarly, splenic phytohemagglutinin (PHA)-induced blastogenesis was significantly depressed at 31 ppm, without a concomitant significant depression in numbers of T-lymphocytes. These data indicate that concentrations of benzene at or near the current standard for occupational exposure (10 ppm) can affect certain immune-associated processes.
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Previous studies have demonstrated that the abnormal fluorescent peak consistent with the crosslinking of red cell membrane constituents by the lipid-peroxide decomposition product MDA is demonstrable in lipid-containing extracts of red cells obtained from patients treated with the oxidizing hemolytic agent diaminodiphenylsulfone. The present studies were primarily aimed at ascertaining the specificity of this fluorescence as an indicator of in vivo red cell lipid peroxidation. Repetitive injection of phenylhydrazine or acetylphenylhydrazine in rats resulted in gradually increasing levels of fluorescence despite the return in hematocrit toward normal. Chromatography on Sephadex LH-20 of lipid-containing extracts obtained from the red cells of rats and rabbits treated with phenylhydrazine revealed fluorescent peaks similar to those observed in red cell lipid incubated with MDA. In addition, increased levels of fluorescence were observed in the extracts of red cells obtained from three vitamin E--deficient premature infants. These findings suggest that the fluorescence assay is a sensitive indicator of in vivo red cell lipid peroxidation.