An evaluation of the dorset sheep as a predictive animal model for the response of G-6-PD deficient human erythrocytes to a proposed systemic toxic ozone intermediate, methyl oleate hydroperoxide.

  title={An evaluation of the dorset sheep as a predictive animal model for the response of G-6-PD deficient human erythrocytes to a proposed systemic toxic ozone intermediate, methyl oleate hydroperoxide.},
  author={Edward J. Calabrese and Gary S. Moore and P S Williams},
  journal={Veterinary and human toxicology},
  volume={25 4},
Erythrocytes of both G-6-PD deficient humans and Dorset sheep, an animal model with an erythrocyte G-6-PD deficiency, both responded in a dose dependent manner to the oxidant stress of MOHP as measured by decreases in G-6-PD activity, increases in METHB levels and decreases in GSH. However, the human G-6-PD deficient erythrocytes were considerably more sensitive to the formation of METHB than the sheep erythrocytes while the reverse was the case for the GSH parameter. The results suggest a… 
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Attempts to validate a possible predictive animal model for human erythrocyte G‐6‐PD deficiency
The results indicated that metabolites of the Pharmaceuticals, B‐naphthol, dapsone, and sulfanilamide, are oxidant, which agreed with studies on the response of human G‐6‐PD deficient erythrocytes.
Use of a bioactivation system to screen for hemolytic response to environmental agents: Evaluation of six pesticides
The pesticides, zineb and parathion, incubated without the microsomal enzyme system, did exert statistically significant oxidizing effects on the G‐6‐PD deficient erythrocytes, in vitro.
Screening for potential hemolytic responses to environmental agents using a bioactivation system: Evaluation of six pesticides
The results indicated that the parent compounds of all the pesticides and the metabolites of all pesticides except diuron were not oxldant stressor agents towards G‐6‐PD deficient erythrocytes, in vitro.
Increased resistance to oxidative stress in normal and glucose-6-phosphate dehydrogenase-deficient hemolysates in the presence of enzyme substrates
Chemiluminescence intensities in erythrocytes of normal and deficient subjects were similar in the presence or absence of glucose-6-phosphate dehydrogenase substrates, but with the addition of substrates to the incubation medium, deficient hemolysates reached maximum chemilumine intensity within a shorter period, and maximum values were higher than in normal hemysates.


Effect ofin vivo ozone exposure to dorset sheep, an animal model with low levels of erythrocyte glucose-6-phosphate dehydrogenase activity
  • G. Moore, E. Calabrese, E. Schulz
  • Biology, Environmental Science
    Journal of environmental pathology, toxicology and oncology : official organ of the International Society for Environmental Toxicology and Cancer
  • 1984
Female Dorset sheep were exposed in vivo to ambient ozone levels and the effects of this exposure upon erythrocytes were studied, showing biochemical evidence of oxidant stress as indicated by decreases in GSH levels and ACHE and increases in MetHb.
The effect of methyl linoleate hydroperoxide (MLHP), a possible toxic intermediate of ozone, on human normal and glucose‐6‐phosphate dehydrogenase (G‐6‐PD) deficient erythrocytes
The G‐ 6‐PD deficient eryth‐rocytes displayed a markedly enhanced sensitivity to MLPH induced decreases in G‐6‐PD activity and METHB increases while being less sensitive than normal erythrocytes to changes in GSH levels.
G6PD-deficiency: a potential high-risk group to copper and chlorite ingestion.
In vitro exposure of G6PD deficient red blood cells to copper produced marked elevations of methemoglobin and decreases in GSH when compared with normal red cells, and chlorite, a by-product of chlorine dioxide disinfection of water, was additive in producing increased levels of hemoglobin and decreased in levels of GSH and G6 PD deficient cells.
Ozone and human blood.
Serum GSSRase activity, however, was significantly decreased while serum vitamin E, and lipid peroxidation levels were significantly increased, and alterations tend to disappear gradually, but were still detectable two weeks following exposure.
Prevention of Ozonide-Induced Heinz Bodies in human Erythrocytes by Vitamin E.
Observations suggest that the protective effects of vitamin E against ozone-produced toxicants occurs in man as well as in animals.
Nutritional needs in environmental intoxication: vitamin E and air pollution, an example.
  • D. Menzel
  • Chemistry
    Environmental health perspectives
  • 1979
Dietary vitamin E affects the susceptibility of mice and rats to ozone and nitrogen dioxide, suggesting a free radical mechanism of toxicity, and the level of vitamin E needed for protection against peroxidation toxicity may be much greater than the present U. S. dietary intake.
Introductory remarks: Session on genetic factors affecting pollutant toxicity.
  • D. Gardner
  • Environmental Science
    Environmental health perspectives
  • 1979
It becomes vitally important to carefully define the population at risk, the mode of exposure, and the lowest concentration that will cause an adverse health effect, because in many instances the action of one toxic agent can be modified by exposure to other agents.