Javier Del Pino
Complutense University, Spain
Title: Sexual and regional permanent dopaminergic system impairment after prenatal and postnatal exposure to chlordimeform
Submitted Date: June 10, 2017
Biography
Javier Del Pino received his PharmD degree from the University Complutense University of Madrid in 2004. He has two Master degrees. He specialized in Neurotoxicology and Neurodevelopmental Toxicology and received his PhD in Toxicology in the year 2009. In 2010, he worked at the Institute of Health Carlos III in the National Center of Environmental Health. From 2010 to 2012, he was an Associated Researcher at University of Massachusetts (UMASS) working in Sandra Petersen’s Lab at a National Institute of Health (NIH) project on developmental effects of TCDD endocrine disruptor on sexual differentiation. In 2016, he became an Associated Professor of Toxicology at the Complutense University of Madrid.
Abstract
Formamidine pesticides induce permanent effects on development of monoaminergic neurotransmitter systems. In this regard, chlordimeform induces permanent sex-dependent alterations of serotoninergic and noradrenergic systems, but there is no information on dopaminergic system. The mechanisms that induce these effects are not known, but it has been suggested that these effects could be related to monoamine oxidase (MAO) inhibition. In order to determine whether chlordimeform induces permanent alterations of dopaminergic system, the effects of maternal exposure to chlordimeform (5 mg/kg bw, orally on days 6–21 of pregnancy and 1–10 of lactation) on dopamine levels in different brain regions of male and female offspring rats at 60 days of age were evaluated by HPLC. Maternal and offspring body weight, physical and general activity developments were unaffected. Our results show that chlordimeform induced a significant decrease of dopamine levels in the prefrontal cortex, hippocampus and striatum, showing a gender interaction for these regions. Chlordimeform also caused a decrease of DOPAC levels in the striatum. Moreover, it induced an increase in the content of metabolites DOPAC and HVA in the hippocampus and an increase in the metabolite content of DOPAC in the striatum. Lastly, it increased the turnover of DA in the hippocampus and striatum and decreased the turnover of DA in frontal cortex. The present findings indicate that maternal exposure to chlordimeform altered dopaminergic neurochemistry in their offspring in a region and sex-dependent way.
Javier Del Pino
Complutense University, Spain
Title: Amitraz alterations in estradiol content in CNS of male rats
Submitted Date: June 10, 2017
Biography
Javier Del Pino received his PharmD degree from the University Complutense University of Madrid in 2004. He has two Master degrees. He specialized in Neurotoxicology and Neurodevelopmental Toxicology and received his PhD in Toxicology in the year 2009. In 2010, he worked at the Institute of Health Carlos III in the National Center of Environmental Health. From 2010 to 2012, he was an Associated Researcher at University of Massachusetts (UMASS) working in Sandra Petersen’s Lab at a National Institute of Health (NIH) project on developmental effects of TCDD endocrine disruptor on sexual differentiation. In 2016, he became an Associated Professor of Toxicology at the Complutense University of Madrid.
Abstract
Amitraz is a formamidine insecticide/acaricide that alters different neurotransmitters levels, among other neurotoxic effects. Oral amitraz exposure (20, 50 and 80 mg/kg bw, 5 days) has been reported to increase serotonin (5-HT), norepinephrine (NE) and dopamine (DA) content and to decrease their metabolites and turnover rates in the male rat brain, particularly in the striatum, prefrontal cortex, and hippocampus. However, the mechanisms by which these alterations are produced are not completely understood. One possibility is that amitraz monoamine oxidase (MAO) inhibition could mediate these effects. Alternatively, it alters serum concentrations of sex steroids that regulate the enzymes responsible for these neurotransmitters synthesis and metabolism. Thus, alterations in sex steroids in the brain could also mediate the observed effects. To test whether amitraz alter sex hormones in the brain, we treated male rats with 20, 50 and 80 mg/kg bw for 5 days and then isolated tissue from striatum, prefrontal cortex, and hippocampus. We then measured plasma and tissue levels of estradiol (E2) and testosterone (T) in these regions. Our results show that Amitraz treatment did not alter the content of E2 in plasma and T in the brain regions studied. However, amitraz induced a dose-dependent increase in T content in plasma and E2 content in the regions of prefrontal cortex, striatum and hippocampus from highest to lowest in this order. Our present results provide new understanding of the mechanisms contributing to the harmful effects of amitraz.
