Gary S. Moore
University of Massachusetts Amherst
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Featured researches published by Gary S. Moore.
Mycologia | 1977
Gary S. Moore; Robin D. Atkins
SUMMARYA variety of yeast-like fungi representing the genera Candida, Cryptococcus, Rhodotorula, Torulopsis, and Trichosporon was inhibited in vitro in the presence of an aqueous extract of garlic....
Environmental Research | 1980
Edward J. Calabrese; Gary S. Moore; Soon-Ching Ho
Abstract The effects of copper on selected characteristics of blood from normal and G-6-PD deficient humans and sheep of the Dorset Strain (which also have comparable red cell G-6-PD activity units as G-6-PD deficient humans) were compared. Both the G-6-PD deficient humans and sheep were found to be markedly more sensitive to several indicators of oxidant stress as measured by increases in methemoglobin levels and decreases in the activity of red cell acetylcholinesterase. These findings indicate that susceptibility to copper-induced oxidative stress is associated with the presence of low red cell G-6-PD activity.
Medical Hypotheses | 1978
Gary S. Moore; Edward J. Calabrese; Salvatore R. DiNardi; Robert W. Tuthill
Chlorination of potable water supplies high in organics may yield carcinogenic compounds such as trihalomethanes. Chlorine dioxide has been proposed as an alternative disinfectant to chlorine. However, chlorine dioxide is a strong oxidant that forms significant amounts of chlorite when added to potable water supplies, and chlorite is similar to nitrite in its molecular structure and may be similar in its mechanism of methemoglobin production. Nitrites and chlorites are thought to act synergistically to produce MetHb. Neonates and persons with G-*-PD deficiency are likely to be unusually susceptible to MetHb formation from these compounds because their red cells lack the metabolic machinery to adequately protect against oxidant stress. Since male blacks represent the largest population in the U.S. to be G-6PD deficient, Black male neonates may represent the group at highest risk to the use of chlorine dioxide as a disinfectant in the nations water supplies.
Medical Hypotheses | 1981
Edward J. Calabrese; Carol Sacco; Gary S. Moore; Salvatore R. DiNardi
It has been hypothesized that sulfite oxidase deficient persons may be at increased risk to toxicity from SO2 and dietary sulfites widely used for food preservation. Sulfite oxidase is believed to be responsible for the detoxification of SO2 and/or sulfite to sulfate for excretion. Human and animal studies have shown that S-sulfonates, believed to transport sulfite in the blood, are formed in response to exposure to low levels of SO2. Besides its numerous toxic effects, e.g. respiratory impairment, interference with immunological response and oxygen transport and platelet aggregation inhibition, SO2 has the ability to alter DNA during replication causing T . A transitions, chromosome abnormalities and depression of DNA synthesis.
Archives of Environmental Health | 1987
Edward J. Stanek; Robert W. Tuthill; Cleve E. Willis; Gary S. Moore
Household wastes, when disposed of improperly, are hazardous to health. This paper reports a random digit dial telephone survey of Massachusetts households concerning household hazardous waste (HHW) disposal with a 54% response. Of the automotive oil disposed of by 33% of survey households, 57% was deposited in the ground, sewer, or landfill. Annually by household oil disposal in Massachusetts is estimated to be 8.8 million quarts. Four percent of hazardous waste generated in Massachusetts is from households. Improper disposal makes it a major environmental contaminant. More households (41.5%) in smaller communities disposed of oil compared with 26% of households in larger communities. Paint and pesticides were disposed of by 10% of the households, but were dumped on the ground sewer or landfills more than 90% of the time.
Regulatory Toxicology and Pharmacology | 1983
Edward J. Calabrese; Gary S. Moore; Mark S. McCarthy
Interspecies differences were demonstrated with respect to the occurrence of sodium nitrite-induced methemoglobin (METHB) in the erythrocytes of rats, dorset sheep, and normal humans, with the rats displaying approximately 25-33% of the sensitivity of sheep and human erythrocytes. Ascorbic acid incubation along with the nitrite was able to significantly reduce METHB formation in a dose-dependent manner in both rats and humans but not in sheep.
Regulatory Toxicology and Pharmacology | 1983
Edward J. Calabrese; Gary S. Moore; Mark S. McCarthy
Rats, sheep, and normal humans displayed a comparable sensitivity to copper acetate (3 mM)-induced changes in reduced glutathione (GSH) levels in vitro. However, the human erythrocytes were more sensitive than either animal to methemoglobin (METHB) formation with the rat being least sensitive. Ascorbic acid incubation markedly enhanced the occurrence of copper acetate-induced increases in METHB and decreases in GSH in the sheep and humans. However, ascorbic acid incubation reduced the occurrence of copper acetate-induced increases in METHB, while not effecting changes in GSH in rats.
Ecotoxicology and Environmental Safety | 1983
Edward J. Calabrese; Perry S. Williams; Gary S. Moore
Erythrocytes of both glucose-6-phosphate dehydrogenase (G-6-PD)-deficient humans and Dorset sheep, an animal model with an erythrocyte G-6-PD deficiency, responded in a dose-dependent manner to the oxidant stress of methyl oleate ozonide (MOO) as measured by decreases in G-6-PD activity, increases in methemoglobin (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 qualitative difference in the response of sheep erythrocytes and human G-6-PD-deficient erythrocytes to MOO that seriously questions the value of the sheep erythrocyte as a quantitatively accurate predictive model.
Journal of Environmental Science and Health Part A-toxic\/hazardous Substances & Environmental Engineering | 1983
Mary Ballew; Edward J. Calabrese; Gary S. Moore
Abstract The present study evaluated the effects of a single three hour ozone exposure on erythrocyte parameters of male Dawkin‐Hartley guinea pigs that were reared on diets high or low in vitamin C for 11 days prior to the ozone exposure. The results indicated that consumption of diets highly different in vitamin C levels did not have a significant effect on ozone induced alterations in erythrocyte parameters although there was a trend toward higher methemoglobin values in the ozone treated guinea pigs reared on the low vitamin C diets as compared to similarly exposed animals given the high vitamin C diet. While ambient ozone (O3) is primarily recognized as a potent respiratory irritant, it is now known that O3 may exert an array of systemic effects including altered liver function,1,2 induction of chromosomal aberrations,3,5 and changes in red cell metabolism.6,7 since O3 is an environmental oxidant, investigators8–11 have assessed the capacity of the dietary antioxidant vitamin E to reduce O3 toxicity....
Ecotoxicology and Environmental Safety | 1983
Edward J. Calabrese; Gary S. Moore; Mark S. McCarthy
Ascorbic acid significantly reduced the occurrence of sodium nitrite-induced methemoglobin (METHB) formation in a dose-dependent manner in erythrocytes from glucose-6-phosphate dehydrogenase (G-6-PD)-deficient humans in vitro. The ascorbic acid treatment, however, also decreased levels of reduced GSH in a dose-dependent manner, a response indicative of oxidant stress to the erythrocyte membrane. The latter findings are inconsistent with the hypothesis that ascorbic acid supplementation in G-6-PD-deficient humans may help compensate for inherently low levels of erythrocyte GSH. Finally, the ascorbic acid-induced reduction of METHB values, while of statistical significance, does not appear to be of clinical significance.