Environmental Toxicology and Pharmacology 43 (2016) 83–93 Contents lists available at ScienceDirect Environmental Toxicology and Pharmacology j o ur na l ho mepage: www.elsevier.com/locate/etap Depletion of mitochondrial enzyme system in liver, lung, brain, stomach and kidney induced by benzo(a)pyrene Xiaoying Ji a,1 , Yongfei Li b,1 , Jianlong He c , Walayat Shah d , Xiaochang Xue e , Guodong Feng f , Huqin Zhang g , Meili Gao a,∗ a Department of Biological Science and Engineering, The Key Laboratory of Biomedical Information Engineering of Ministry of Education, School of Life Science and Technology, Xi’an Jiaotong University, 710049, China b School of Materials and Chemical Engineering, Xi’an Technological University, Xi’an 710032, China c Xi’an Jiaotong University, Xi’an 710049, China d Institute of Basic Medical Sciences, Khyber Medical University, Peshawar, Pakistan e State Key Laboratory of Cancer Biology, Department of Biopharmaceutics School of Pharmacy, Fourth Military Medical University, Xi’an, Shaanxi 710032, China f Department of Neurology, Xijing Hospital, Fourth Military Medical University, 17 Changle West Road, Shaanxi, Xi’an 710032, China g The Key Laboratory of Biomedical Information Engineering of Ministry of Education, School of Life Science and Technology, Xi’an Jiaotong University, Xi’an 710049, China a r t i c l e i n f o Article history: Received 30 August 2015 Received in revised form 25 February 2016 Accepted 2 March 2016 Available online 4 March 2016 Keywords: Benzo(a)pyrene Depletion of mitochondrial enzymes Histopathological lesion Multiple organs a b s t r a c t Mitochondrial dysfunction has recently received considerable attention as it plays an important role in adult human pathology caused by various drugs, endogenous agents and environmental agents. Benzo(a)pyrene (BaP), is a ubiquitous environmental contaminant mainly derived from anthropogenic activity during incomplete combustion of organic materials from various sources. The present study aimed to evaluate the effects of benzo(a)pyrene (BaP) on mitochondrial enzymes in the multiple organs including liver, lung, brain, stomach and kidney. ICR mice were exposed to different doses of BaP (2.5, 5 and 10 mg/kg body weight) through oral gavage and intraperitoneal injection treatment for 13 weeks consecutively. The induced mitochondrial damage in the examined organs was assayed in terms of signif- icant increase in lipid peroxidation (LPO) and prominent decrease in antioxidant enzymes. Non enzymatic antioxidants and Krebs cycle’s enzymes were also significantly decreased in mitochondria. Additionally, BaP induced the body growth retardation and decrease in relative liver weight, increase in relative lung, stomach, kidney and brain weights, and this was further certified through histopathological lesions. Liver and lungs were more prominently damaged by BaP. The mitochondrial depletion increased in BaP dose-dependent manner. © 2016 Elsevier B.V. All rights reserved. 1. Introduction Mitochondria play an important role in converting organic materials into cellular energy in the adenosine triphosphate (ATP) form via oxidative phosphorylation and supply the cell with ATP to meet the bulk of needs. Studies have indicated that mitochondria are essential for cell life and decision-makers regulating cell death. Simultaneously, mitochondria are an important cellular source of oxygen radicals and are more easily affected by free radical attack to ∗ Corresponding author at: Department of Biological Science and Engineering, School of Life Science and Technology, Xi’an Jiaotong University, 710049 Xi’an, China. E-mail address: gaomeili@mail.xjtu.edu.cn (M. Gao). 1 These are co-first authors cause mitochondrial dysfunction (Kamaraj et al., 2011; Priya et al., 2011; Yang et al., 2011). Mitochondrial dysfunction has recently received considerable attention as it plays an important role in adult human pathology caused by various drugs, other endogenous agents and environmental agents (Priya et al., 2011). Benzo(a) pyrene (BaP), a kind of polycyclic aromatic hydrocar- bons (PAHs), is a ubiquitous environmental contaminant mainly derived from anthropogenic activity during incomplete combus- tion of organic materials from various sources (Hattemer-Frey and Travis, 1991). It is metabolically activated into phenols, epoxides, dihydrodiols, dihydrodiol epoxides, quinones, and the ultimate carcinogenic metabolite anti-7,8-dihydroxy-9,10-epoxy- 7,8,9,10-tetrahydro-BaP (BPDE) by both phase I and phase II biotransformation enzymes. Simultaneously, BaP is metabolized by cytochrome P-450 (CYP), especially CYP1A1, 1B1 epoxide hydrolase http://dx.doi.org/10.1016/j.etap.2016.03.001 1382-6689/© 2016 Elsevier B.V. All rights reserved.