Time course of inhibition of cholinesterase and aliesterase activities, and nonprotein sulfhydryl levels following exposure to organophosphorus insecticides in mosquitofish (Gambusia affinis)

被引:46
作者
Boone, JS [1 ]
Chambers, JE [1 ]
机构
[1] MISSISSIPPI STATE UNIV,DEPT BIOL SCI,MISSISSIPPI STATE,MS 39762
来源
FUNDAMENTAL AND APPLIED TOXICOLOGY | 1996年 / 29卷 / 02期
关键词
D O I
10.1006/faat.1996.0023
中图分类号
R99 [毒物学(毒理学)];
学科分类号
100405 ;
摘要
Cholinesterase (ChE) in brain and muscle was quickly inhibited during a 48-hr in vivo exposure to chlorpyrifos (0.1 ppm), parathion (0.15 ppm), and methyl parathion (8 ppm) in mosquitofish (Gambusia affinis). ChE remained inhibited during a 96-hr nonexposure period. Brain ChE reached peak inhibition by 12 hr after exposure to parathion and chlorpyrifos and by 4 hr after exposure to methyl parathion. All insecticides caused greater than 70% ChE inhibition by 4 hr in muscle. There was no recovery of ChE after 4 days of nonexposure in either brain or muscle, Hepatic aliesterases (AliE) were quickly and greatly inhibited (>70% by 4 hr) after exposure to parathion and chlorpyrifos but not after exposure to methyl parathion, Exposure to methyl parathion required 24-36 hr to inhibit hepatic AliE to the same level as that following parathion and chlorpyrifos exposures at 4 hr. Exposure to all insecticides eventually resulted in greater than 80% inhibition of AliE. None of the test groups treated with insecticides showed any signs of significant recovery of AliE during the 4 days of nonexposure. Nonprotein sulfhydryl (NPSH) concentrations were lower than controls after 24 hr of exposure and 96 hr after recovery for all compounds. Exposure to methyl parathion lowered NPSH concentrations greater than the other compounds. Hepatic AliE appear capable of affording some protection of ChE from inhibition following parathion or chlorpyrifos exposures, but considerably less protection against methyl parathion. (C) 1996 Society of Toxicology
引用
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页码:202 / 207
页数:6
相关论文
共 37 条
[1]  
[Anonymous], 1980, Reviews in Biochemical Toxicology
[2]   ANTICHOLINESTERASE ACTION OF METHYL PARATHION, PARATHION AND AZINPHOSMETHYL IN MICE AND FISH - ONSET AND RECOVERY OF INHIBITION [J].
BENKE, GM ;
MURPHY, SD .
BULLETIN OF ENVIRONMENTAL CONTAMINATION AND TOXICOLOGY, 1974, 12 (01) :117-122
[3]   COMPARATIVE TOXICITY, ANTICHOLINESTERASE ACTION AND METABOLISM OF METHYL PARATHION AND PARATHION IN SUNFISH AND MICE [J].
BENKE, GM ;
CHEEVER, KL ;
MIRER, FE ;
MURPHY, SD .
TOXICOLOGY AND APPLIED PHARMACOLOGY, 1974, 28 (01) :97-109
[4]   EFFECT OF SOME CARBONYL COMPOUNDS ON RAT LIVER GLUTATHIONE LEVELS [J].
BOYLAND, E ;
CHASSEAUD, LF .
BIOCHEMICAL PHARMACOLOGY, 1970, 19 (04) :1526-+
[5]   ACUTE EFFECTS OF THE ORGANOPHOSPHATE PARAOXON ON SCHEDULE-CONTROLLED BEHAVIOR AND ESTERASE-ACTIVITY IN RATS - DOSE-RESPONSE RELATIONSHIPS [J].
CARR, RL ;
CHAMBERS, JE .
PHARMACOLOGY BIOCHEMISTRY AND BEHAVIOR, 1991, 40 (04) :929-936
[6]   AN INVESTIGATION OF ACETYLCHOLINESTERASE INHIBITION AND AGING AND CHOLINE-ACETYLTRANSFERASE ACTIVITY FOLLOWING A HIGH-LEVEL ACUTE EXPOSURE TO PARAOXON [J].
CHAMBERS, HW ;
CHAMBERS, JE .
PESTICIDE BIOCHEMISTRY AND PHYSIOLOGY, 1989, 33 (02) :125-131
[7]  
CHAMBERS HW, 1990, PEST BICOH PHYSL, V36, P162
[8]   ROLE OF DETOXICATION PATHWAYS IN ACUTE TOXICITY LEVELS OF PHOSPHOROTHIONATE INSECTICIDES IN THE RAT [J].
CHAMBERS, JE ;
MA, TG ;
BOONE, JS ;
CHAMBERS, HW .
LIFE SCIENCES, 1994, 54 (18) :1357-1364
[9]   PARATHION AND METHYL PARATHION TOXICITY TO INSECTICIDE-RESISTANT AND SUSCEPTIBLE MOSQUITOFISH (GAMBUSIA-AFFINIS) [J].
CHAMBERS, JE ;
YARBROUGH, JD .
BULLETIN OF ENVIRONMENTAL CONTAMINATION AND TOXICOLOGY, 1974, 11 (04) :315-320
[10]   TIME COURSE OF INHIBITION OF ACETYLCHOLINESTERASE AND ALIESTERASES FOLLOWING PARATHION AND PARAOXON EXPOSURES IN RATS [J].
CHAMBERS, JE ;
CHAMBERS, HW .
TOXICOLOGY AND APPLIED PHARMACOLOGY, 1990, 103 (03) :420-429