INHIBITION AND AGING OF CHANNEL CATFISH BRAIN ACETYLCHOLINESTERASE FOLLOWING EXPOSURE TO 2 PHOSPHOROTHIONATE INSECTICIDES AND THEIR ACTIVE METABOLITES

被引:13
作者
CARR, RL [1 ]
STRAUS, DL [1 ]
CHAMBERS, JE [1 ]
机构
[1] MISSISSIPPI STATE UNIV,COLL VET MED,CTR ENVIRONM HLTH SCI,MISSISSIPPI STATE,MS 39762
来源
JOURNAL OF TOXICOLOGY AND ENVIRONMENTAL HEALTH | 1995年 / 45卷 / 03期
关键词
D O I
10.1080/15287399509531999
中图分类号
X [环境科学、安全科学];
学科分类号
08 ; 0830 ;
摘要
The inhibition and aging of acetylcholinesterase (AChE) in fingerling channel catfish (Ictalurus punctatus) brain tissue was studied after single in vivo exposures to high levels of chlorpyrifos (0.25 mg/L), chlorpyrifos-oxon (7 mu g/L), parathion (2.5 mg/L), or paraoxon (30 mu g/L). Exposure to both parent compounds produced identical initial inhibition (95%), but in the later sampling times there was significantly more inhibited AChE in the chlorpyrifos-treated fish than in the parathion-treated fish (47% and 28%, respectively, on d 16). There were higher levels of aged AChE following chlorpyrifos exposure than following parathion exposure, but differences were not significant. Exposure to both oxons produced initial inhibition greater than 90%, and patterns of recovery and aging were statistically similar between both compounds; no significant inhibition was observed after d ii. The similar patterns of inhibition, recovery, and aging between the two oxon treatments, which have similar lipophilicities, suggest that the greater amount of AChE inhibition and aging observed in the chlorpyrifos-treated fish compared with the parathion-treated fish probably results from the higher lipophilicity of chlorpyrifos than of parathion. Overall, the prolonged brain AChE inhibition exhibited in catfish exposed to phosphorothionates is not the result of aging of the inhibited enzyme but is the result of either a slow rate or a lack of spontaneous reactivation.
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页码:325 / 336
页数:12
相关论文
共 25 条
[1]  
BARRON MG, 1993, ENVIRON TOXICOL CHEM, V12, P1469, DOI [10.1897/1552-8618(1993)12[1469:ATDAMO]2.0.CO
[2]  
2, 10.1002/etc.5620120814]
[3]   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
[4]   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
[5]  
BOONE JS, 1991, THESIS MISSISSIPPI S
[6]   AGEING AND REACTIVATION OF ACETYLCHOLINESTERASE INHIBITED WITH SOMAN AND ITS THIOCHOLINE-LIKE ANALOGUE [J].
BOSKOVIC, B ;
MAKSIMOVIC, M ;
MINIC, D .
BIOCHEMICAL PHARMACOLOGY, 1968, 17 (08) :1738-+
[7]  
CARR RL, 1992, TOXICOLOGIST, V12, P42
[8]   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
[9]   INHIBITION PATTERNS OF BRAIN ACETYLCHOLINESTERASE AND HEPATIC AND PLASMA ALIESTERASES FOLLOWING EXPOSURES TO 3 PHOSPHOROTHIONATE INSECTICIDES AND THEIR OXONS IN RATS [J].
CHAMBERS, JE ;
CARR, RL .
FUNDAMENTAL AND APPLIED TOXICOLOGY, 1993, 21 (01) :111-119
[10]  
CHAMBERS JE, 1988, NEUROSCI RES COMMUN, V3, P85