Parental and preimaginal exposure to methylmercury disrupts locomotor activity and circadian rhythm of adult Drosophila melanogaster

Abstract

Methylmercury (MeHg) is a well-known toxic pollutant. However, little is known about the effects of this toxic agent in an adult as a consequence of a parental or preimaginal exposure. This study used Drosophila melanogaster to investigate whether a parental or a preimaginal (eggs–larvae–pupae stages) exposure could impact parameters as viability, locomotor activity, and sleep patterns of fruit flies. Thus, we performed two exposure protocols. One where just parents were exposed to MeHg (0–12 µM) during 24 h, then flies were transferred to lay eggs in a healthy medium (without MeHg). In the other, flies were set to lay eggs in a MeHg medium, same concentrations, and discarded after this (preimaginal exposure). Viability was evaluated from egg to adult flies. F1 progeny was collected within 24 h and transferred to a fresh healthy medium. Sleep behavior analysis was performed using Drosophila Active Monitoring System (DAMS), and the locomotor activity was evaluated by climbing assay. Results have shown that the parental exposure had a significant impact on F1 progeny reducing viability and locomotor activity performance, but no significant circadian rhythm alterations. Whereas the preimaginal exposure had a stronger effect decreasing viability and locomotor activity, it also disrupted sleep patterns. MeHg preimaginal exposure showed a longer sleep duration and lower daily activity. Results corroborate the hypothesis that low MeHg exposure could trigger subclinical symptoms related to a ‘neurotoxicological development effect’. Complementary investigations could clarify the underlying mechanisms of MeHg effects in neural functions due to parental and early development exposure to this toxicant.

Keywords:

• Heavy metal toxicity
• neurotoxicity
• neuromuscular dysfunction
• climbing assay
• sleep behavior disruption
• sleep–waking activity
• daytime and nighttime activity

Acknowledgements

The authors also would like to thank the Laboratory of Cellular Genetics team for support and technical assistance.

Disclosure statement

No potential conflict of interest was reported by the authors.

Additional information

Funding

This study was supported by the collaboration between the Japan Science and Technology Agency (JST) and the Japan Agency for Medical Research and Development (AMED) – JST/AMED – # JP16jm0310022; and by the National Council for Scientific and Technological Development (CNPq) # 490760/2013-9. Also, the graduate fellowship by the Brazilian Federal Agency for Graduate Education (CAPES) and CNPq. Funding sources had no role in study design; in the collection, analysis and interpretation of data; in the writing of the manuscript; and in the decision to submit the article for publication.