In vivo metabolic fate of [14C]-acetamiprid in six biological compartments of the honeybee, Apis mellifera L

被引:89
作者
Brunet, JL [1 ]
Badiou, A [1 ]
Belzunces, LP [1 ]
机构
[1] UAPV, INRA, UMR 406, Lab Toxicol Environm, F-84914 Avignon, France
关键词
acetamiprid; metabolite; honeybee; metabolism; biodistribution; neonicotinoid;
D O I
10.1002/ps.1046
中图分类号
S3 [农学(农艺学)];
学科分类号
0901 ;
摘要
The in vivo metabolism of acetamiprid was studied in the honeybee, Apis mellifera L. The distribution of acetamiprid and its metabolites was monitored over a 72-h period in six biological compartments: head, thorax, abdomen, haemolymph, midgut and rectum. Honeybees were treated orally with 100 mu g [C-14]-acetamiprid kg(-1) bee, a dose which is about 1500 times lower than the median lethal dose. After 72 h, only 40% of the total radioactivity was eliminated, suggesting that acetamiprid and its metabolites tended to persist in the honeybee. Acetamiprid was rapidly distributed in all compartments and metabolized. just after administration, radioactivity was mainly localized in the abdomen and subsequently in the rectum. After 72 h, the maximum amount of radioactivity (about 20% of the ingested dose) was detected again in the abdomen, whereas the lowest level of total radioactivity was detected in the haemolymph. Radioactivity in the head did not exceed 7.6% of total ingested radioactivity. More than 50% of acetamiprid was metabolised in less than 30 min, indicating a very short half-life for the compound. During the first hours, acetamiprid was mainly detected in nicotinic acetylcholine receptor-rich tissues: abdomen, thorax and head. Of the seven metabolites detected, the major ones were 6-choronicotinic acid and an unknown metabolite called U1, which was present mainly in the rectum, the thorax and the head. Our results indicate that the low toxicity of acetamiprid may reflect its rapid metabolism. (c) 2005 Society of Chemical Industry.
引用
收藏
页码:742 / 748
页数:11
相关论文
共 55 条
[1]  
*ARLA, 2002, REG200205 ARLA USEPA
[2]   IN-VITRO INHIBITION OF MIDGUT MICROSOMAL P450S FROM SPODOPTERA-ERIDANIA CATERPILLARS BY DEMETHYLATION INHIBITOR FUNGICIDES AND PLANT-GROWTH REGULATORS [J].
BRATTSTEN, LB ;
BERGER, DA ;
DUNGAN, LB .
PESTICIDE BIOCHEMISTRY AND PHYSIOLOGY, 1994, 48 (03) :234-243
[3]   Human intestinal absorption of imidacloprid with Caco-2 cells as enterocyte model [J].
Brunet, JL ;
Maresca, M ;
Fantini, J ;
Belzunces, LP .
TOXICOLOGY AND APPLIED PHARMACOLOGY, 2004, 194 (01) :1-9
[4]   Translocation and translaminar bioavailability of two neonicotinoid insecticides after foliar application to cabbage and cotton [J].
Buchholz, A ;
Nauen, R .
PEST MANAGEMENT SCIENCE, 2002, 58 (01) :10-16
[5]  
Deng YeCheng, 2002, Southwest China Journal of Agricultural Sciences, V15, P50
[6]  
*EPPO, 1992, EPPO B, V23, P203
[7]   ASSESSMENT OF CHRONIC TOXICITY OF SELECTED INSECTICIDES TO HONEYBEES [J].
FIEDLER, L .
JOURNAL OF APICULTURAL RESEARCH, 1987, 26 (02) :115-122
[8]   Comparative toxicity of foliar and systemic applications of acetamiprid and imidacloprid against the cotton whitefly, Bemisia tabaci (Hemiptera: Aleyrodidae) [J].
Horowitz, AR ;
Mendelson, Z ;
Weintraub, PG ;
Ishaaya, I .
BULLETIN OF ENTOMOLOGICAL RESEARCH, 1998, 88 (04) :437-442
[9]  
Illarionov AI, 1991, AGROKHIMIVA, V8, P121
[10]  
Ishaaya Isaac, 2001, Mededelingen Faculteit Landbouwkundige en Toegepaste Biologische Wetenschappen Universiteit Gent, V66, P363