Possible involvement of oxidative stress in piperonyl butoxide induced hepatocarcinogenesis in rats

Muguruma, Masako; Unami, Akira; Kanki, Masayuki; Kuroiwa, Yoshihiro; Nishimura, Jihei; Dewa, Yasuaki; Umemura, Takashi; Oishi, Yuji; Mitsumori, Kunitoshi

doi:10.1016/j.tox.2007.03.025

Cited by 71 publications

(33 citation statements)

References 39 publications

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“…Therefore, CYP1A inducers are known to generate large amount of ROS. In addition, it has been demonstrated that CYP1A inducers such as piperonyl butoxide, oxfendazole and β-naphthoflavone can generate ROS via a metabolic pathway in the livers of rats, which induces oxidative stress that is involved in hepatocarcinogenesis (Dewa et al, 2009;Muguruma et al, 2007). Similarly, PB, a CYP2B1/2 inducer, has been shown to increase hydroxyl radical levels in the livers of rats Waxman et al, 1992).…”

Section: Discussionmentioning

confidence: 99%

Liver tumor promoting effect of orphenadrine in rats and its possible mechanism of action including CAR activation and oxidative stress

et al. 2013

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Section: Discussionmentioning

confidence: 99%

Liver tumor promoting effect of orphenadrine in rats and its possible mechanism of action including CAR activation and oxidative stress

et al. 2013

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“…These changes seem to be related to PBO pretreatment. Muguruma et al (66) reported that PBO increased microsomal ROS production in the liver. This suggests that lower TBARS levels in the present study could be attributed to lower tGSH levels that act against ROS production.…”

Section: Effects Of Pbo On Imi Toxicitymentioning

confidence: 99%

Sex-, tissue-, and exposure duration-dependent effects of imidacloprid modulated by piperonyl butoxide and menadione in rats. Part I: oxidative and neurotoxic potentials

Yardimci

Sevgiler

Rencüzoğulları

et al. 2014

Archives of Industrial Hygiene and Toxicology

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Earlier research has evidenced the oxidative and neurotoxic potential of imidacloprid, a neonicotinoid insecticide, in different animal species. The primary aim of this study was to determine how metabolic modulators piperonyl butoxide and menadione affect imidacloprid's adverse action in the liver and kidney of Sprague-Dawley rats of both sexes. The animals were exposed to imidacloprid alone (170 mg kg -1 ) or in combination with piperonyl butoxide (100 mg kg -1 ) or menadione (25 mg kg -1 ) for 12 and 24 h. Their liver and kidney homogenates were analysed spectrophotometrically for glutathione peroxidase, glutathione S-transferase, catalase, total cholinesterase specific activities, total glutathione, total protein content, and lipid peroxidation levels. Imidacloprid displayed its prooxidative and neurotoxic effects predominantly in the kidney of male rats after 24 h of exposure. Our findings suggest that the observed differences in prooxidative and neurotoxic potential of imidacloprid could be related to differences in its metabolism between the sexes. Co-exposure (90-min pre-treatment) with piperonyl butoxide or menadione revealed tissue-specific effect of imidacloprid on total cholinesterase activity. Increased cholinesterase activity in the kidney could be an adaptive response to imidacloprid-induced oxidative stress. In the male rat liver, co-exposure with piperonyl butoxide or menadione exacerbated imidacloprid toxicity. In female rats, imidacloprid+menadione co-exposure caused prooxidative effects, while no such effects were observed with imidacloprid alone or menadione alone. In conclusion, sex-, tissue-, and duration-specific effects of imidacloprid are remarkable points in its toxicity.

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“…mangano-type superoxide dismutase, catalase, or glutathione peroxidase) may not be directly associated with cancer risk, it is possible that accumulative defects in protection from oxidative stress may result in increased risk of the disease (Ryter et al, 2007). Piperonyl butoxide (PBO), is a pesticide widely used along with pyrethroids as grain protector and domestic insecticide (Muguruma et al, 2007). PBO is capable of increasing the gene expression of CYP1A1, a cytochrome P-450 isoform and the most active enzyme catalyzing procarcinogens (Canistro et al, 2002).…”

Section: Cancermentioning

confidence: 99%

“…PBO is capable of increasing the gene expression of CYP1A1, a cytochrome P-450 isoform and the most active enzyme catalyzing procarcinogens (Canistro et al, 2002). PBO has a liver-tumor-promoting effect increasing production of ROS as a byproduct of hepatic microsomal oxidation in mice (Muguruma et al, 2007). The increase of ROS is due to PBO-induced regulation of glutathione reductase (GR), NADPH: quinone oxidoreductase 1 (NQO 1 ), and other antioxidant enzymes.…”

Section: Cancermentioning

confidence: 99%

Molecular Mechanisms of Pesticide Toxicity

Tebourbi¹,

Sakly²,

Rhouma³

2011

Pesticides in the Modern World - Pests Control and Pesticides Exposure and Toxicity Assessment

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Possible involvement of oxidative stress in piperonyl butoxide induced hepatocarcinogenesis in rats

Cited by 71 publications

References 39 publications

Liver tumor promoting effect of orphenadrine in rats and its possible mechanism of action including CAR activation and oxidative stress

Liver tumor promoting effect of orphenadrine in rats and its possible mechanism of action including CAR activation and oxidative stress

Sex-, tissue-, and exposure duration-dependent effects of imidacloprid modulated by piperonyl butoxide and menadione in rats. Part I: oxidative and neurotoxic potentials

Molecular Mechanisms of Pesticide Toxicity

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