Abstract
BackgroundMany pesticides have been shown to act as endocrine disrupters. Although the potencies of currently used pesticides as hormone agonists/antagonists are low compared with those of natural ligands, their ability to act via multiple mechanisms might enhance the biological effect. The organophosphate Chlorpyrifos (CHP) has been shown to be weakly estrogenic and cause adverse neurodevelopmental effects in mammals. However, no information is available on the endocrine effects of CHP in aquatic organisms. In the digestive gland of the bivalve Mytilus galloprovincialis, a target tissue of both estrogens and pesticides, the possible effects of CHP on the responses to the natural estrogen 17β-estradiol (E2) were investigated.Methodology/Principal FindingsMussels were exposed to CHP (4.5 mg/l, 72 hrs) and subsequently injected with E2 (6.75 ng/g dw). Responses were evaluated in CHP, E2 and CHP/E2 treatment groups at 24 h p.i. by a biomarker/transcriptomic approach. CHP and E2 induced additive, synergistic, and antagonistic effects on lysosomal biomarkers (lysosomal membrane stability, lysosome/cytoplasm volume ratio, lipofuscin and neutral lipid accumulation). Additive and synergistic effects were also observed on the expression of estrogen-responsive genes (GSTπ, catalase, 5-HTR) evaluated by RT-Q-PCR. The use of a 1.7K cDNA Mytilus microarray showed that CHP, E2 and CHP/E2, induced 81, 44, and 65 Differentially Expressed Genes (DEGs), respectively. 24 genes were exclusively shared between CHP and CHP/E2, only 2 genes between E2 and CHP/E2. Moreover, 36 genes were uniquely modulated by CHP/E2. Gene ontology annotation was used to elucidate the putative mechanisms involved in the responses elicited by different treatments.ConclusionsThe results show complex interactions between CHP and E2 in the digestive gland, indicating that the combination of certain pesticides and hormones may give rise to unexpected effects at the molecular/cellular level. Overall, these data demonstrate that CHP can interfere with the mussel responses to natural estrogens.
Highlights
Many endocrine-disrupting compounds (EDCs) so far identified are persistent organochlorine pesticides (e.g., DDT, methoxychlor, dieldrin) [1]
CHP induced a significant increase in neutral lipid (NL) content; a smaller effect was observed in response to E2 (+27%)
The results presented in this work indicate that CHP exposure affects the responses of mussel digestive gland to the natural estrogen E2
Summary
Many endocrine-disrupting compounds (EDCs) so far identified are persistent organochlorine pesticides (e.g., DDT, methoxychlor, dieldrin) [1]. Modern pesticides, such as most organophosphates, do not bioaccumulate and they might not reach concentrations able to cause endocrine disruption in humans or wildlife. The potencies of pesticides as estrogen agonists/antagonists and antiandrogens in vitro are low compared with those of natural ligands [7]. Chemicals with similar estrogenic potencies in vitro sometimes show very different potencies in vivo [8] Their ability to act via more than one mechanism might enhance the biological effect in the intact organism, since the final response will likely be determined by the interactions of all pathways implicated. The potencies of currently used pesticides as hormone agonists/antagonists are low compared with those of natural ligands, their ability to act via multiple mechanisms might enhance the biological effect. In the digestive gland of the bivalve Mytilus galloprovincialis, a target tissue of both estrogens and pesticides, the possible effects of CHP on the responses to the natural estrogen 17b-estradiol (E2) were investigated
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