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Toxicology

Title:		Exposure to arsenic during embryogenesis impairs olfactory sensory neuron differentiation and function into adulthood
Author(s):		Szymkowicz DB; Sims KC; Schwendinger KL; Tatnall CM; Powell RR; Bruce TF; Bridges WC; Bain LJ;
Address:		"Environmental Toxicology Graduate Program, Clemson University, Clemson, SC, USA. Department of Biological Sciences, Clemson University, Clemson, SC, USA. Clemson Light Imaging Facility, Clemson University, Clemson, SC, USA. School of Mathematical and Statistical Sciences, Clemson University, Clemson, SC, USA. Environmental Toxicology Graduate Program, Clemson University, Clemson, SC, USA; Department of Biological Sciences, Clemson University, Clemson, SC, USA. Electronic address: lbain@clemson.edu"
Journal Title:		Toxicology
Year:		2019
Volume:		20190410
Issue:
Page Number:		73 - 84
DOI:		10.1016/j.tox.2019.04.005
ISSN/ISBN:		1879-3185 (Electronic) 0300-483X (Print) 0300-483X (Linking)
Abstract:		"Arsenic is a contaminant of food and drinking water. Epidemiological studies have reported correlations between arsenic exposure and neurodevelopmental abnormalities, such as reduced sensory functioning, while in vitro studies have shown that arsenic reduces neurogenesis and alters stem cell differentiation. The goal of this study was assess whether arsenic exposure during embryogenesis reduced olfactory stem cell function and/or numbers, and if so, whether those changes persist into adulthood. Killifish (Fundulus heteroclitus) embryos were exposed to 0, 10, 50 or 200 ppb arsenite (As(III)) until hatching, and juvenile fish were raised in clean water. At 0, 2, 4, 8, 16, 28 and 40 weeks of age, odorant response tests were performed to assess specific olfactory sensory neuron (OSN) function. Olfactory epithelia were then collected for immunohistochemical analysis of stem cell (Sox2) and proliferating cell numbers (PCNA), as well as the number and expression of ciliated (calretinin) and microvillus OSNs (G(alphai3)) at 0, 4, 16 and 28 weeks. Odorant tests indicated that arsenic exposure during embryogenesis increased the start time of killifish responding to pheromones, and this altered start time persisted to 40 weeks post-exposure. Response to the odorant taurocholic acid (TCA) was also reduced through week 28, while responses to amino acids were not consistently altered. Immunohistochemistry was used to determine whether changes in odorant responses were correlated to altered cell numbers in the olfactory epithelium, using markers of proliferating cells, progenitor cells, and specific OSNs. Comparisons between response to pheromones and PCNA + cells indicated that, at week 0, both parameters in exposed fish were significantly reduced from the control group. At week 28, all exposure are still significantly different than control fish, but now with higher PCNA expression coupled with reduced pheromone responses. A similar trend was seen in the comparisons between Sox2-expressing progenitor cells and response to pheromones, although Sox2 expression in the 28 week-old fish only recovers back to the level of control fish rather than being significantly higher. Comparisons between calretinin expression (ciliated OSNs) and response to TCA demonstrated that both parameters were reduced in the 200 ppb arsenic-exposed fish in at weeks 4, 16, and 28. Correlations between TCA response and the number of PCNA + cells revealed that, at 28 weeks of age, all arsenic exposure groups had reductions in response to TCA, but higher PCNA expression, similar to that seen with the pheromones. Few changes in G(alphai3) (microvillus OSNs) were seen. Thus, it appears that embryonic-only exposure to arsenic has long-term reductions in proliferation and differentiation of olfactory sensory neurons, leading to persistent effects in their function"
Keywords:		"Animals Arsenites/*toxicity Behavior, Animal/drug effects Calbindin 2/metabolism Embryo, Nonmammalian/*drug effects/metabolism Female Fish Proteins/metabolism Fundulidae/*embryology/metabolism Male Neurogenesis/*drug effects Odorants Olfactory Receptor Ne;"
Notes:		"MedlineSzymkowicz, Dana B Sims, Kaleigh C Schwendinger, Katey L Tatnall, Caroline M Powell, Rhonda R Bruce, Terri F Bridges, William C Bain, Lisa J eng P20 GM109094/GM/NIGMS NIH HHS/ P20 RR021949/RR/NCRR NIH HHS/ R03 ES023930/ES/NIEHS NIH HHS/ Research Support, N.I.H., Extramural Research Support, U.S. Gov't, Non-P.H.S. Ireland 2019/04/13 Toxicology. 2019 May 15; 420:73-84. doi: 10.1016/j.tox.2019.04.005. Epub 2019 Apr 10"