Cytogenetic and developmental toxicity of bisphenol A and bisphenol S in Arbacia lixula sea urchin embryos

Bisphenol S (BP-S) is one of the most important substitutes of bisphenol A (BP-A), and its environmental occurrence is predicted to intensify in the future. Both BP-A and BP-S were tested for adverse effects on early life stages of Arbacia lixula sea urchins at 0.1 up to 100 mu M test concentrations, by evaluating cytogenetic and developmental toxicity endpoints. Embryonic malformations and/or mortality were scored to determine embryotoxicity (72 h post-fertilization). It has been reported in academic dataset that bisphenols concentration reached mu g/L in aquatic environment of heavily polluted areas. We have chosen concentrations ranging from 0.1-100 mu M in order to highlight, in particular, BP-S effects. Attention should be paid to this range of concentrations in the context of the evaluation of the toxicity and the ecological risk of BP-S as emerging pollutant. Cytogenetic toxicity was measured, using mitotic activity and chromosome aberrations score in embryos (6 h post-fertilization). Both BP-A and BP-S exposures induced embryotoxic effects from 2.5 to 100 mu M test concentrations as compared to controls. Malformed embryo percentages following BP-A exposure were significantly higher than in BP-Sexposed embryos from 0.25 to 100 mu M (with a similar to 5-fold difference). BP-A, not BP-S exhibited cytogenetic toxicity at 25 and 100 mu M. Our results indicate an embryotoxic potential of bisphenols during critical periods of development with a potent rank order to BP-A vs. BP-S. Thus, we show that BP-A alternative induce similar toxic effects to BP-A with lower severity.Faculty of Fisheries, Ege University; Tunisian Ministry of Higher Education and Scientific Research; Universita degli Studi di Napoli Federico II within the CRUI-CARE AgreementThis work was supported by Faculty of Fisheries, Ege University and The Tunisian Ministry of Higher Education and Scientific Research. Open access funding provided by Universita degli Studi di Napoli Federico II within the CRUI-CARE Agreement

Protective effects of caffeic acid against hypothalamic neuropeptides alterations induced by malathion in rat

International audienceExposure to pesticides is suspected to cause human health problems. Our study aimed to evaluate preventive effects of caffeic acid (3,4-dihydroxycinnamic acid) in the hypothalamus against malathion-induced neuropeptides gene expression alterations. Malathion at 100 mg/kg was administered intragastrically to rats alone or in combination with caffeic acid at 100 mg/kg during 4 weeks. A molecular expression of hypothalamic neuropeptides and plasmatic cholinesterase activity was investigated. Furthermore, we used in silico analysis, known as computational docking, to highlight the nature of acetylcholinesterase-malathion/caffeic acid interactions. Our findings showed differences in the responses and indicate that caffeic acid reversed malathion-induced decrease in corticotropin-releasing hormone mRNA but not brain-derived neurotrophic factor which presented an increased tendency. We suggest that caffeic acid can interact with acetylcholinesterase as the primary target of organophosphorus compounds. Results predict that caffeic acid can block partly the acetylcholinesterase gorge entrance via π-π stacking interaction with Tyr 124 and Trp 286 residues of the peripheral site leading to its stricture. Under this condition, we suggested that acetylcholine trafficking toward the catalytic site is ameliorated compared to malaoxon according to their size