Sublethal exposures of diazinon alters glucose homostasis in Wistar rats: Biochemical and molecular evidences of oxidative stress in adipose tissues

作者: Mohsen Pakzad , Shamileh Fouladdel , Amir Nili-Ahmadabadi , Nazila Pourkhalili , Maryam Baeeri

DOI: 10.1016/J.PESTBP.2012.11.008

关键词: Adipose tissueBiologyInternal medicineOxidative stressInsulinEndocrinologyGlucose homeostasisDiazinonGLUT4Glucose transporterNADPH oxidaseAgronomy and Crop ScienceHealth, Toxicology and MutagenesisGeneral Medicine

摘要: Abstract Disorder of glucose homeostasis is one the most important complications following exposure to organophosphorous (OPs) pesticides. Regarding importance adipose tissue in regulating blood and role oxidative stress toxicity OPs continue our previous works, present study we focused on tumor necrosis factor alpha (TNFα), transporter type 4 (GLUT4), nuclear kappa-light-chain-enhancer activated B cells (Nf-κB) a sublethal model by diazinon as common OPs. Following time-course various doses impairing glucose, dose 70 mg/kg/day was found optimum. Animals were treated for 4 weeks after gavage (2 g/kg), change evaluated at time-points 0, 30, 60, 120 180 min identify oral tolerance test (GTT). In addition, serum insulin measured fasting condition. tissue, markers including reactive oxygen species (ROS), nicotinamide adenine dinucleotide phosphate (NADPH) oxidase TNFα evaluated. The mRNA expression GLUT4, Nf-κB glyceraldehyde 3-phosphate dehydrogenase (GAPDH) also determined real time reverse transcription polymerase chain reaction (RT-PCR). Diazinon impaired GTT diminished level while augmented ROS, NADPH oxidase, TNFα. GLUT4 amplified unlikely, gene did not change. On basis biochemical molecular findings, it concluded that impairs through related proinflammatory way result reduced function inside tissue. Although, interfered with pancreatic influence probably via stimulation muscarinic receptors, current data are sufficient introduce target organ toxicity. Considering potential accumulate seems good candidate future studies. hyperglycemia induced but increased AUC 0–180 min leads us point induces kind instability homostasis diabetes.

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