Contribution of monoaminergic nervous system in potentiation of 2-sec-butylphenylN-methylcarbamate (BPMC) toxicity by malathion in male mice |
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| Affiliation: | 1. School of Nursing, Jilin University, Changchun, Jilin, 130021, China;2. Department of Hematology, Qingdao Municipal Hospital, Qingdao, Shandong, 261041, China;3. Department of Surgery, University of Pittsburgh, Pittsburgh, PA, 15213, USA;4. Center for DAMP Biology, The Third Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong, 510150, China;1. Jiangsu Collaborative Innovation Center of Atmospheric Environment and Equipment Technology, Jiangsu Key Laboratory of Atmospheric Environment Monitoring and Pollution Control, Nanjing University of Information Science & Technology, 219 Ningliu Road, Nanjing 210044, China;2. State Key Laboratory of Pollution Control and Resource Reuse, School of the Environment, Nanjing University, Nanjing 210023, China;3. National Institute of Environmental Health, Chinese Center for Disease Control and Prevention, Beijing, China;4. Yale Center on Climate Change and Health, Yale School of Public Health, 60 College Street, New Haven, CT 06520-8034, USA;5. Department of Epidemiology and Environmental Health, School of Public Health and Health Professions, University at Buffalo, Buffalo, NY, USA;6. RENEW Institute, University at Buffalo, Buffalo, NY, USA;7. Department of Environmental and Occupational Health Sciences, School of Public Health, University of Washington, Seattle, WA, USA |
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| Abstract: | Malathion-induced marked potentiation of BPMC toxicity (about fivefold) was analyzed by measuring LD50 as an index of acute toxicity. The acute lethality of BPMC was decreased by muscarinic blockers (atropine, methylatropine, or trihexyphenidyl) or a monoamine oxidase inhibitor (pargyline) and increased by a monoamine depleter (reserpine) or a dopaminergic blocker (haloperidol). The potentiation observed with BPMC and malathion was decreased by the muscarinic blockers, monoamine depleters (reserpine, α-methyl-p-tyrosine), an α-noradrenergic blocker (phentolamine), or haloperidol. The acute toxicities of other N-methylcarbamates MPMC (3,4-dimethylphenyl N-methylcarbamate), MTMC (3-methylphenyl N-methylcarbamate), NAC (1-naphthyl N-methylcarbamate), and XMC (3,5-dimethylphenyl N-methylcarbamate) were potentiated by malathion to a lesser degree than that of BPMC. Atropine protected against the lethalities of all N-methylcarbamates. Reserpine or haloperidol potentiated the lethalities of N-methylcarbamates with a similar tendency toward malathion. When the inhibitory effect of each N-methylcarbamate on brain acetylcholinesterase (AChE) was compared with its LD50, among five N-methylcarbamates BPMC had particularly strong anti-AChE activity. This characteristic of BPMC was not observed after the treatment with reserpine. These results suggest that BPMC may act not only on cholinergic nerves as an anti-AChE, but also on monoaminergic nerves which antagonize the lethal cholinergic effect. Malathion might inhibit the effect of BPMC on the monoaminergic nerves, thereby markedly potentiating the lethal effect of BPMC. |
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