Organophosphate Pesticide Exposure and Glucose Homeostasis
Journal Title: Biomedical Journal of Scientific & Technical Research (BJSTR) - Year 2019, Vol 14, Issue 2
Abstract
Present review discusses the organophosphate (OP) pesticides toxicity with associated hyperglycemia in animal as well as human studies and effect of OP pesticide on liver enzymes involved in glucose homeostasis pathways. Pancreas keeps hormonal control of glucose homeostasis by secretion of glucagon and insulin. Insulin resistance is higher risk of impair glucose homeostasis. Based on cumulative evidences, oxidative stress induced by OP pesticides may lead to disturbance of glucose homeostasis. There is increasing interest in environment pesticides exposure can affect the glucose homeostasis. Introduction Organophosphate (OP) compounds have been used as pesticides since 1975. OP insecticide compounds are a diverse group of chemicals. This compound contains different group of chemicals such as acephate, diazinon, dimethorate, parathion, phosmet, malathion, parathion, diazinon, fenthion, dichlorvos, chlorpyrifos, ethion, azamethiphos [1]. There is emerging evidence that OP has various toxicities such as neurotoxicity, endocrine toxicity, immunotoxicity, reproductive toxicity, genotoxicity and cellular oxidative imbalance and impaired glucose homeostasis at the hazard of human and animal health. It was found the notable coincidence of occurrences in association between OP poisoning and severe hyperglycemia. Two patients, mother and son presented with many complicated symptoms including hyperglycemia and administration of pralidoxime (AChE activator) normalized blood glucose level. Though acetylcholinesterase enzyme level had not been detected in these patients, they had history of exposure to malathion sprayed in their area [2]. Many case report studies had described the detail sign and symptoms of OP pesticide poisoning accompanying hyperglycemia. Then , it has been raised awareness of association between OP poisoning and severe hyperglycemia in human. Effect of OP Pesticide on Liver Enzymes Involved in Glucose Homeostasis Pathways Culminating hyperglycemia has been increasingly reported as outcome of OP poisoned animal model studies. Exposure of rats to OP compounds such as Malathion [3-5], acephate [6] and dimethoate [7] developed hyperglycemia with stimulation of hepatic gluconeogenesis and glycogenolysis. The possible mechanism of increase blood glucose level might be due to stimulation of hepatic gluconeogenesis and glycogenolysis for increased energy production to detoxification. Upon entering the body– through contact with skin and mucous membrane, inhalation and ingestion– OP pesticides avidly binds the AChE by forming covalent bond between OP pesticides and oxygen of serine at the active site of AChE then it transforms into irreversible phosphorylated inactive AChE and lead to increased acetylcholine activity [8,9]. Thus, hyperesthesia, intermittent spasm, muscular tremors, sustained seizures and muscle fasciculation are induced by cholinergic action of OP pesticides [10]. These involuntary energy demanding activities trigger the release of glucose by glycogenolysis and gluconeogenesis. It also stimulates the glycolysis of liver and muscle, and subsequent releases of ATP to meet the body’s energy requirement [4,11]. Effect of OP Pesticide Exposure on Oxidative Stress Exposure to OP pesticides, inhibits the AChE enzyme and increases the activity of muscarinic type of Ach receptor. The overstimulation of Ach receptors result in uncoordinated nerve and muscle stimulation leading to sustained seizures and muscle fasciculation [10]. During these conditions, the flow of oxygen through brain and muscle is greatly increased. This metabolic stress results in increase requirement the ATPs for them and increase demand of glucose, which in turn activates the glycolysis. Glycolysis is oxygen independent metabolic pathway that converts glucose into pyruvate. This process releases the high energy molecule ATP (adenosine triphosphate) and NADH (reduced nicotinamide adenine dinucleotide) [12,13]. These products of glycolysis are oxidized by using atmospheric oxygen.
Authors and Affiliations
Mya Thanda Sein, Mya Pwint Phyu
Keywords
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- EP ID EP594314
- DOI 10.26717/BJSTR.2019.14.002525
- Views 183
- Downloads 0
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