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Phoxim‐induced damages of Bombyx mori larval midgut and titanium dioxide nanoparticles protective role under phoxim‐induced toxicity
Author(s) -
Su Junju,
Li Bing,
Cheng Shen,
Zhu Zhou,
Sang Xuezi,
Gui Suxin,
Xie Yi,
Sun Qingqing,
Cheng Zhe,
Cheng Jie,
Hu Rengping,
Shen Weide,
Xia Qingyou,
Zhao Ping,
Hong Fashui
Publication year - 2014
Publication title -
environmental toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.813
H-Index - 77
eISSN - 1522-7278
pISSN - 1520-4081
DOI - 10.1002/tox.21866
Subject(s) - phoxim , superoxide dismutase , chemistry , glutathione , glutathione reductase , oxidative stress , antioxidant , biochemistry , reactive oxygen species , bombyx mori , malondialdehyde , toxicity , glutathione peroxidase , pharmacology , toxicology , biology , enzyme , pesticide , organic chemistry , gene , agronomy
Phoxim ( O , O ‐diethyl O ‐(alpha‐cyanobenzylideneamino) phosphorothioate) is a powerful organophosphorus pesticide with high potential for Bombyx mori larvae of silkworm exposure. However, it is possible that during the phoxim metabolism, there is generation of reactive oxygen species (ROS) and phoxim may produce oxidative stress and neurotoxicity in an intoxicated silkworm. Titanium dioxide nanoparticles (TiO 2 NPs) pretreatment has been demonstrated to increase antioxidant capacity and acetylcholinesterase (AChE) activity in organisms. This study was, therefore, undertaken to determine phoxim‐induced oxidative stress and neurotoxicity to determine whether phoxim intoxication alters the antioxidant system and AChE activity in the B. mori larval midgut, and to determine whether TiO 2 NPs pretreatment attenuates phoxim‐induced toxicity. The findings suggested that phoxim exposure decreased survival of B. mori larvae, increased malondialdehyde (MDA), carbonyl and 8‐OHdG levels, and ROS accumulation in the midgut. Furthermore, phoxim significantly decreased the activities of AChE, superoxide dismutase (SOD), ascorbate peroxidase (APX), glutathione reductase (GR), glutathione‐ S ‐transferase (GST), and levels of ascorbic acid (AsA), reduced glutathione (GSH), and thiol in the midgut. TiO 2 pretreatment, however, could increase AChE activity, and remove ROS via activating SOD, CAT, APX, GR, and GST, and accelerating AsA–GSH cycle, thus attenuated lipid, protein, and DNA peroxidation and improve B. mori larval survival under phoxim‐induced toxicity. Moreover, this experimental system would help nanomaterials to be applied in the sericulture. © 2013 Wiley Periodicals, Inc. Environ Toxicol 29: 1355–1366, 2014.