4.7 Article

The insecticides chlorpyrifos and acetamiprid induce redox imbalance in umbilical cord blood erythrocytes in vitro

期刊

PESTICIDE BIOCHEMISTRY AND PHYSIOLOGY
卷 148, 期 -, 页码 87-92

出版社

ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.pestbp.2018.04.001

关键词

Umbilical cord blood; Pesticides; Chlorpyrifos; Acetamiprid; Oxidative Stress

资金

  1. Consejo National de Investigaciones Cientificas y Tecnologicas (CONICET) [PIP2014 0707]
  2. Universidad Nacional del Comahue [04-NO21]

向作者/读者索取更多资源

Organophosphate and neonicotinoid compounds belong to different pesticide families, and are used worldwide for agricultural purposes. The potential deleterious health effects associated with pesticide exposure during pregnancy have become a major public health concern. The present study analyzed the effects of the organophosphate chlorpyrifos and the neonicotinoid acetamiprid on oxidative stress biomarkers in human umbilical cord blood erythrocytes (UCBE). The reactive oxygen species (ROS) levels, the catalase (CAT) and superoxide dismutase (SOD) activities, the levels of 4-hidroxynonenal (HNE) and UCBE osmotic fragility were determined. Both pesticides modified the oxidative status of UCBE. Chlorpyrifos increased ROS levels at 40 and 400 nM, while only decreased CAT activity at the higher concentration assayed (400 nM), with no modification in SOD activity. The insecticide acetamiprid increased ROS levels at all concentrations assayed, and decreased CAT and SOD activity at 40 and 400 nM, Chlorpyrifos and acetamiprid (40 and 400 nM) modified HNE content. Nonsignificant changes in UCBE osmotic fragility were induced by chlorpyrifos or acetamiprid treatments. In conclusion, both pesticides assayed increased ROS production and decreased anti-oxidant enzyme activity in UCBE, even though changes were of different extent and depended on the insecticide analyzed. Interestingly no changes in erythrocyte osmotic fragility were registered; suggesting that the oxidative stress triggered under these experimental conditions was not sufficient to induce a functional damage to the UCBE membrane.

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