Article
Physiological and biochemical effects of acute exposure of fish to hydrogen sulfide.
Agricultural Research Center, University of Arkansas at Pine Bluff, Pine Bluff, AR 71601, U.S.A.; Department of Zoology, University of Oklahoma, Norman, OK 73069, U.S.A.
Comparative Biochemistry and Physiology Part C Comparative Pharmacology
02/1982;
71(2):183-90.
DOI:10.1016/0306-4492(82)90034-X
pp.183-90
Source: PubMed
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Article: Toxicology of hydrogen sulfide.
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ABSTRACT: Significant progress has been made in determining the action of sulfide on the primary target organs. It is reasonably clear that sulfide causes both K(+)-channel-mediated hyperpolarization of neurons and potentiation of other inhibitory mechanisms. It is not clear whether these processes are similar to those that occur in anoxia. Changes in perinatal and adult brain neurotransmitter content and release may be related to clinical impairment of cognition. H2S exposures at concentrations below the current occupational limits cause physiological changes in pulmonary function, thus suggesting that asthmatics are at risk. Studies of fetal and neonatal brain tissue have shown an abnormal development, and the long-term consequences of these neuronal changes have not yet been assessed. Finally, new approaches to therapy are required, such as the use of agents that actively remove sulfide from its sites of action. This may prove more useful in preventing some of the long-term adverse sequelae than the use of nitrites and hyperbaric O2, although the latter should be used in cases of pulmonary edema.Annual Review of Pharmacology 02/1992; 32:109-34. · 21.64 Impact Factor
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Keywords
10 degrees C. 6. Management practices
20 degrees C
50% inhibition
blood lactate
Catfish
Catfish brain cytochrome oxidase activity
channel catfish
commercial fish farmer
control fish
control levels
cytochrome oxidase activity
freshwater
gill cytochrome oxidase
harvest operations
hydrogen sulfide
inhibition
nitrite-induced methemoglobinemia
respiratory arrest
Sulfide-inhibited brain cytochrome oxidase
toxicity