PubMed · 781893
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A N Kudrin, T A Babkina, Iu V Pashin. 1976. [Current problems in pharmacogenetics].. https://pubmed.ncbi.nlm.nih.gov/781893/
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Two Hungarian acatalasemic and eight hypocatalasemic patients revealed normal erythropoesis. Contrary to their decreased defence system against the toxic hydrogen peroxide, the biochemical tests (serum catalase, serum hemoglobin, serum lactate dehydrogenase (LDH) ratio of LDH1 and LDH2 isoenzymes and serum haptoglobin) excluded hemolysis. The normal activity of glutathione peroxidase and the decreased catalase activity could prevent the lysis of the erythrocytes. In the presence of extremely high levels of hydrogen peroxide acute hemolysis may not be excluded; therefore, follow-up of these patients is required.
To clarify the role of catalase, an antioxidant enzyme, in response to UV irradiation, we compared the effects of irradiation on cytotoxicity, activities of antioxidant enzymes, total glutathione concentrations, lipid peroxidation and the rate of collagen synthesis in skin fibroblasts from a patient with acatalasaemia and in those from a normal individual. The cells were irradiated with UVA (6 and 12 J/cm2 or UVB (0.5 and 1 J/cm2). Cell survival curves after UV irradiation were similar in cells from both subjects. Although superoxide dismutase activity in acatalasaemia cells was higher than in the control cells before irradiation, after irradiation the activity decreased in acatalasaemia cells (76% with 12 J/cm2 UVA, 47% with 1 J/cm2 UVB), but remained unchanged in control cells. Total glutathione concentrations also decreased in acatalasaemia cells (60% with 12 J/cm2) in response to UVA irradiation, but remained unchanged in control cells. Lipid peroxidation did not increase significantly in either cell type. The rate of collagen synthesis decreased to a similar extent in response to UV exposure in the two cell types (60-80% with 8.2 J/cm2 UVA, 40-50% with 10 mJ/cm2 UVB). We conclude from the results of cytotoxicity and lipid peroxidation that although acatalasaemia cells were killed by hydrogen peroxide at low concentrations with a single UV exposure, catalase functions only to a small degree as an antioxidant enzyme. There remains the possibility, however, that a deficiency of catalase may chronically damage the skin resulting in a reduced defence function of superoxide dismutase and glutathione with repeated exposures to UV, which is becoming more common in our daily life.
To investigate the role of hydrogen peroxide in Cr(VI) toxicity in vivo toward bacterial cells, we examined the effect of Cr(VI), hydrogen peroxide, sodium azide, and mannitol on the viability of Escherichia coli. Bacterial cells were incubated for 1 h with shaking in the presence of Cr(VI), hydrogen peroxide, sodium azide as catalase inhibitor, and/or mannitol as radical scavenger. The colony-forming ability and double-strand DNA degradation were examined. The viability assays revealed that Cr(VI) toxicity depended on hydroxyl radicals generated in the reaction involving hydrogen peroxide and chromium. Moreover, incubation of E. coli cells with 10 mM Cr(VI) and 3 mM hydrogen peroxide caused the degradation of double-strand DNA in vivo, which was suppressed by the addition of mannitol. These results indicated that hydroxyl radicals generated in the incubation degraded DNA of E. coli cells, resulting in cell death. In the absence of added hydrogen peroxide, the intracellular concentration of hydrogen peroxide in E. coli was low (below 1 microM). A catalase-defective strain incubated in the absence of added hydrogen peroxide remained fully viable after 1 h but showed decreased viability after prolonged incubation (4-8 h). The addition of mannitol suppressed this decrease, suggesting that hydroxyl radicals may be involved in the expression of Cr(VI) toxicity even without added hydrogen peroxide.