棉花学报
棉花學報
면화학보
COTTON SCIENCE
2008年
4期
249-255
,共7页
棉铃虫%交互抗性%抗性机理%酯酶%多功能氧化酶
棉鈴蟲%交互抗性%抗性機理%酯酶%多功能氧化酶
면령충%교호항성%항성궤리%지매%다공능양화매
Helicoverpa armigera Hübner%cross-resistance%resistance mechanism%esterase%mixed function oxidase
用辛硫磷/氟氯氰菊酯(25:1, 有效成分)混剂对棉铃虫田间种群(HN)进行33代筛选获得抗性品系(HN-R).筛选获得的HN-R抗性品系对辛硫磷和氟氯氰菊酯的抗性分别达17.4倍和144.7倍.HN-R品系对两种拟除虫菊酯产生了高水平交互抗性(对氯氰菊酯和氰戊菊酯分别为86.2和23.4倍),对久效磷产生了中等水平交互抗性(5.2倍),对甲基对硫磷(1.6倍)、丙溴磷(1.8倍)和灭多威(2.4倍)产生了低水平交互抗性.酯酶抑制剂DEF能有效抑制HN-R品系对辛硫磷的抗性(增效比为15.3倍),而多功能氧化酶抑制剂PBO则对辛硫磷没有任何增效作用;PBO则使HN-R品系对3种拟除虫菊酯的抗性显著降低(对氟氯氰菊酯、溴氰菊酯和氰戊菊酯的增效比分别为21.9、19.1和21.4倍).DEF和PBO都能使HN-R对久效磷的抗性下降一半(增效比分别为2.2和2.5倍).HN-R抗性品系多功能氧化酶活性(以pNA为底物)和酯酶活性(以a-NA为底物)分别为HN品系的6.5倍和1.6倍.因此,在HN-R抗性品系中至少存在2种代谢抗性机理,即增强的酯酶解毒代谢(对辛硫磷、久效磷)和多功能氧化酶介导的氧化解毒代谢(对3种拟除虫菊酯、久效磷).本研究表明,在田间使用有机磷/拟除虫菊酯混剂可能同时选择出多种代谢抗性机理,从而导致广谱的交互抗性.
用辛硫燐/氟氯氰菊酯(25:1, 有效成分)混劑對棉鈴蟲田間種群(HN)進行33代篩選穫得抗性品繫(HN-R).篩選穫得的HN-R抗性品繫對辛硫燐和氟氯氰菊酯的抗性分彆達17.4倍和144.7倍.HN-R品繫對兩種擬除蟲菊酯產生瞭高水平交互抗性(對氯氰菊酯和氰戊菊酯分彆為86.2和23.4倍),對久效燐產生瞭中等水平交互抗性(5.2倍),對甲基對硫燐(1.6倍)、丙溴燐(1.8倍)和滅多威(2.4倍)產生瞭低水平交互抗性.酯酶抑製劑DEF能有效抑製HN-R品繫對辛硫燐的抗性(增效比為15.3倍),而多功能氧化酶抑製劑PBO則對辛硫燐沒有任何增效作用;PBO則使HN-R品繫對3種擬除蟲菊酯的抗性顯著降低(對氟氯氰菊酯、溴氰菊酯和氰戊菊酯的增效比分彆為21.9、19.1和21.4倍).DEF和PBO都能使HN-R對久效燐的抗性下降一半(增效比分彆為2.2和2.5倍).HN-R抗性品繫多功能氧化酶活性(以pNA為底物)和酯酶活性(以a-NA為底物)分彆為HN品繫的6.5倍和1.6倍.因此,在HN-R抗性品繫中至少存在2種代謝抗性機理,即增彊的酯酶解毒代謝(對辛硫燐、久效燐)和多功能氧化酶介導的氧化解毒代謝(對3種擬除蟲菊酯、久效燐).本研究錶明,在田間使用有機燐/擬除蟲菊酯混劑可能同時選擇齣多種代謝抗性機理,從而導緻廣譜的交互抗性.
용신류린/불록청국지(25:1, 유효성분)혼제대면령충전간충군(HN)진행33대사선획득항성품계(HN-R).사선획득적HN-R항성품계대신류린화불록청국지적항성분별체17.4배화144.7배.HN-R품계대량충의제충국지산생료고수평교호항성(대록청국지화청무국지분별위86.2화23.4배),대구효린산생료중등수평교호항성(5.2배),대갑기대류린(1.6배)、병추린(1.8배)화멸다위(2.4배)산생료저수평교호항성.지매억제제DEF능유효억제HN-R품계대신류린적항성(증효비위15.3배),이다공능양화매억제제PBO칙대신류린몰유임하증효작용;PBO칙사HN-R품계대3충의제충국지적항성현저강저(대불록청국지、추청국지화청무국지적증효비분별위21.9、19.1화21.4배).DEF화PBO도능사HN-R대구효린적항성하강일반(증효비분별위2.2화2.5배).HN-R항성품계다공능양화매활성(이pNA위저물)화지매활성(이a-NA위저물)분별위HN품계적6.5배화1.6배.인차,재HN-R항성품계중지소존재2충대사항성궤리,즉증강적지매해독대사(대신류린、구효린)화다공능양화매개도적양화해독대사(대3충의제충국지、구효린).본연구표명,재전간사용유궤린/의제충국지혼제가능동시선택출다충대사항성궤리,종이도치엄보적교호항성.
Selection of a field strain of Helicoverpa armigera (HN) was undertaken by treatment with a mixture of an organophosphate (phoxim) + a pyrethroid (cyhalothrin) (25:1, a.i.) for 33 generations. The resistance to phoxim of the selected strain (HN-R) increased to 17.4-fold and the resistance to cyhalothrin increased to 144.7-fold. High level cross-resistance to two pyrethroids was detected (86.2-fold to deltamethrin and 23.4-fold to fenvalerate) in the HN-R strain. In addition, the HN-R strain also possessed a moderate level of cross-resistance to monocrotophos (5.2-fold), a low level cross-resistance to methyl parathion(1.6-fold), profenofos (1.8-fold), and methomyl (2.4-fold). The esterase inhibitor S,S,S-tributylphosphorotrithioate (DEF) was very effective in reducing phoxim resistance of the HN-R strain (with a synergism ratio of 15.3-fold) but the mixed function oxidase (MFO) inhibitory synergist piperonyl butoxide (PBO) had no synergism to it at all. In contrast, PBO dramatically removed most of resistance to three pyrethroids with synergism ratios of 21.9-fold to cyhalothrin, 19.1-fold to deltamethrin, and 21.4-fold to fenvalerate, but DEF had no synergism to them. Both DEF and PBO can remove about half of the resistance to monocrotophos (with synergism ratio of 2.2- and 2.5-fold, respectively). Compared to the reference HN strain, the MFO activity of the resistant HN-R strain to p-nitroanisole (pNA) was 6.5-fold and total esterase activity to 1-naphthyl acetate (a-NA) was 1.6-fold. At least two metabolic resistance mechanisms are involved in this resistant HN-R strain: esteratic detoxification (to phoxim and monocrotophos) and oxidative metabolism by mixed function oxidases (to pyrethroids and monocrotophos). The results suggest the use of pyrethroid/organophosphate mixtures in the field is likely to lead the simultaneous selection of multiple metabolic mechanisms of resistance, and thus a broad cross-resistance spectrum.
