title: Glucose-rich diet aggravates monocrotophos-induced dopaminergic neuronal dysfunction in Caenorhabditis elegans.
abstract: The present study aimed to obtain insights into the mechanism(s) by which glucose-rich diet aggravates monocrotophos (MCP)-induced dopaminergic neuronal dysfunction in Caenorhabditis elegans. In this study, we exposed three different strains of worms (wild-type N2, CB1112 (cat-2(e1112)II, tyrosine hydroxylase-deficient mutant, catecholamine absent) and the transgenic BZ555 (egls1-dat-1p::green fluorescent protein [GFP]) (in which bright GFP is tagged to the dopamine neuronal soma and processes) grown and maintained in normal nematode growth medium or 2% glucose enriched-nematode growth medium to MCP (0.75 mm) for 48 h. After the exposure, dopamine-mediated behaviors such as repulsion to nonanone, chemotaxis index and basal slowing response were determined in worms. Dopamine, 3,4-dihydroxy phenyl acetic acid and homovanillic acid content were quantified in N2 worms. The extent of neurodegeneration was visualized and quantified in dat-1::GFP worms. Basal slowing response study clearly indicated that cat-2 worms exposed to MCP and glucose were less affected compared to N2 of the same treatment. Learning and memory were affected by MCP and glucose. While MCP-treated worms showed lesser repulsion to nonanone compared to control worms, MCP-treated, glucose-fed worms showed a greater reduction in repulsion to nonanone. Further, MCP-treated, glucose-fed worms exhibited a marked reduction in dopamine content and an increase in 3,4-dihydroxy phenyl acetic acid and homovanillic acid levels compared to that in control. Dat-1::GFP showed a significant degeneration of dopaminergic neurons when exposed to glucose and MCP. Thus, our results clearly demonstrate that glucose-rich diet aggravates the dopaminergic neuronal dysfunction induced by MCP in C. elegans. Copyright © 2016 John Wiley & Sons, Ltd.
authors.affiliation: Academy of Scientific and Innovative Research (AcSIR), Anusandhan Bhawan, New Delhi, India; Food Protectants and Infestation Control Department, CSIR-Central Food Technological Research Institute, Mysore, 570 020, India.
authors.forename: Chinnu
authors.initials: C
authors.lastname: Salim
authors.affiliation: Academy of Scientific and Innovative Research (AcSIR), Anusandhan Bhawan, New Delhi, India; Food Protectants and Infestation Control Department, CSIR-Central Food Technological Research Institute, Mysore, 570 020, India.
authors.forename: P S
authors.initials: PS
authors.lastname: Rajini
mesh_terms: D000818:Animals; D030801:Animals, Genetically Modified; D001522:Behavior, Animal / Q000187:drug effects*; D017173:Caenorhabditis elegans / Q000187:drug effects* / Q000235:genetics / Q000502:physiology; D002374:Catalase / Q000378:metabolism; D002395:Catecholamines / Q000378:metabolism; D004032:Diet; D004298:Dopamine / Q000378:metabolism; D059290:Dopaminergic Neurons / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D005947:Glucose / Q000633:toxicity*; D049452:Green Fluorescent Proteins / Q000235:genetics; D018613:Microscopy, Confocal; D008856:Microscopy, Fluorescence; D008999:Monocrotophos / Q000633:toxicity*
chemical_list: D002395:Catecholamines; D049452:Green Fluorescent Proteins; D008999:Monocrotophos; D002374:Catalase; D005947:Glucose; D004298:Dopamine
keywords: Caenorhabditis elegans; dopamine; glucose; monocrotophos; neurodegeneration