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NADPH oxidase mediated maneb- and paraquat-induced oxidative stress in rat polymorphs: Crosstalk with mitochondrial dysfunction.
Pestic Biochem Physiol. 2015 Sep; 123:74-86.PB

Abstract

Oxidative stress is a key factor in Parkinson's disease (PD) pathogenesis. Nicotinamide adenine dinucleotide phosphate (NADPH) oxidase and impaired mitochondrion regulate oxidative stress-mediated maneb (MB)- and paraquat (PQ)-induced Parkinsonism. However, their contribution in the MB- and PQ-induced toxicity in polymorphonuclear leukocytes (PMNs) is still elusive. The study investigated the role of NADPH oxidase and mitochondria in MB- and/or PQ-induced oxidative stress in the PMNs and the crossing point between the two. Animals were treated with MB and/or PQ for 1-3 weeks along with respective controls. In a few sets of experiments, rats were treated with/without NADPH oxidase inhibitor, apocynin, an hour prior to MB and/or PQ treatment. PMNs of MB and/or PQ treated animals were also treated with/without carbonyl cyanide 3-chlorophenylhydrazone (CCCP) to assess the role of the mitochondria in superoxide and total free radical productions. MB and/or PQ were found to increase the level of total reactive oxygen species (ROS), superoxide radicals, catalytic activity and expression of NADPH oxidase and superoxide dismutase (SOD1/2) and mitochondrial ROS content in a time dependent manner. Conversely, catalase activity and mitochondrial membrane potential were attenuated. Apocynin alleviated MB- and/or PQ-induced changes in total ROS, superoxide radicals, expression/catalytic activity of NADPH oxidase and SOD1/2 along with the mitochondrial ROS and membrane potential. CCCP also inhibited ROS and superoxide levels in the PMNs of MB and/or PQ-treated animals. The results demonstrate the involvement of NADPH oxidase and mitochondrial dysfunction in MB and PQ-induced oxidative stress in PMNs and a plausible crosstalk between them.

Authors+Show Affiliations

CSIR-Indian Institute of Toxicology Research, Lucknow 226 001, Uttar Pradesh, India.CSIR-Indian Institute of Toxicology Research, Lucknow 226 001, Uttar Pradesh, India; Academy of Scientific and Innovative Research (AcSIR), India.CSIR-Indian Institute of Toxicology Research, Lucknow 226 001, Uttar Pradesh, India; Academy of Scientific and Innovative Research (AcSIR), India.CSIR-Indian Institute of Toxicology Research, Lucknow 226 001, Uttar Pradesh, India; Academy of Scientific and Innovative Research (AcSIR), India.CSIR-Indian Institute of Toxicology Research, Lucknow 226 001, Uttar Pradesh, India.CSIR-Indian Institute of Toxicology Research, Lucknow 226 001, Uttar Pradesh, India.Banaras Hindu University, Varanasi 221 005, Uttar Pradesh, India.CSIR-Indian Institute of Toxicology Research, Lucknow 226 001, Uttar Pradesh, India; Academy of Scientific and Innovative Research (AcSIR), India. Electronic address: singhchetnaitrc@rediffmail.com.

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

26267055

Citation

Shukla, Smriti, et al. "NADPH Oxidase Mediated Maneb- and Paraquat-induced Oxidative Stress in Rat Polymorphs: Crosstalk With Mitochondrial Dysfunction." Pesticide Biochemistry and Physiology, vol. 123, 2015, pp. 74-86.
Shukla S, Singh D, Kumar V, et al. NADPH oxidase mediated maneb- and paraquat-induced oxidative stress in rat polymorphs: Crosstalk with mitochondrial dysfunction. Pestic Biochem Physiol. 2015;123:74-86.
Shukla, S., Singh, D., Kumar, V., Chauhan, A. K., Singh, S., Ahmad, I., Pandey, H. P., & Singh, C. (2015). NADPH oxidase mediated maneb- and paraquat-induced oxidative stress in rat polymorphs: Crosstalk with mitochondrial dysfunction. Pesticide Biochemistry and Physiology, 123, 74-86. https://doi.org/10.1016/j.pestbp.2015.03.007
Shukla S, et al. NADPH Oxidase Mediated Maneb- and Paraquat-induced Oxidative Stress in Rat Polymorphs: Crosstalk With Mitochondrial Dysfunction. Pestic Biochem Physiol. 2015;123:74-86. PubMed PMID: 26267055.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - NADPH oxidase mediated maneb- and paraquat-induced oxidative stress in rat polymorphs: Crosstalk with mitochondrial dysfunction. AU - Shukla,Smriti, AU - Singh,Deepali, AU - Kumar,Vinod, AU - Chauhan,Amit Kumar, AU - Singh,Shweta, AU - Ahmad,Israr, AU - Pandey,Haushila Prasad, AU - Singh,Chetna, Y1 - 2015/03/21/ PY - 2015/02/16/received PY - 2015/03/17/revised PY - 2015/03/17/accepted PY - 2015/8/13/entrez PY - 2015/8/13/pubmed PY - 2016/6/3/medline KW - Maneb KW - Mitochondrial dysfunction KW - NADPH oxidase KW - Oxidative stress KW - Paraquat SP - 74 EP - 86 JF - Pesticide biochemistry and physiology JO - Pestic Biochem Physiol VL - 123 N2 - Oxidative stress is a key factor in Parkinson's disease (PD) pathogenesis. Nicotinamide adenine dinucleotide phosphate (NADPH) oxidase and impaired mitochondrion regulate oxidative stress-mediated maneb (MB)- and paraquat (PQ)-induced Parkinsonism. However, their contribution in the MB- and PQ-induced toxicity in polymorphonuclear leukocytes (PMNs) is still elusive. The study investigated the role of NADPH oxidase and mitochondria in MB- and/or PQ-induced oxidative stress in the PMNs and the crossing point between the two. Animals were treated with MB and/or PQ for 1-3 weeks along with respective controls. In a few sets of experiments, rats were treated with/without NADPH oxidase inhibitor, apocynin, an hour prior to MB and/or PQ treatment. PMNs of MB and/or PQ treated animals were also treated with/without carbonyl cyanide 3-chlorophenylhydrazone (CCCP) to assess the role of the mitochondria in superoxide and total free radical productions. MB and/or PQ were found to increase the level of total reactive oxygen species (ROS), superoxide radicals, catalytic activity and expression of NADPH oxidase and superoxide dismutase (SOD1/2) and mitochondrial ROS content in a time dependent manner. Conversely, catalase activity and mitochondrial membrane potential were attenuated. Apocynin alleviated MB- and/or PQ-induced changes in total ROS, superoxide radicals, expression/catalytic activity of NADPH oxidase and SOD1/2 along with the mitochondrial ROS and membrane potential. CCCP also inhibited ROS and superoxide levels in the PMNs of MB and/or PQ-treated animals. The results demonstrate the involvement of NADPH oxidase and mitochondrial dysfunction in MB and PQ-induced oxidative stress in PMNs and a plausible crosstalk between them. SN - 1095-9939 UR - https://www.unboundmedicine.com/medline/citation/26267055/NADPH_oxidase_mediated_maneb__and_paraquat_induced_oxidative_stress_in_rat_polymorphs:_Crosstalk_with_mitochondrial_dysfunction_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0048-3575(15)00061-9 DB - PRIME DP - Unbound Medicine ER -