Mercury Concentration, DNA Methylation, and Mitochondrial DNA Damage in Olive Ridley Sea Turtle Embryos With Schistosomus Reflexus Syndrome

Abstract

Schistosomus reflexus syndrome (SR) is a rare and lethal congenital malformation that has been reported in the olive ridley sea turtle ( Lepidochelys olivacea) in Mexico. Although the etiology remains unclear, it is presumed to be genetic. Since embryonic development in sea turtles largely depends on environmental conditions, we investigated whether sea turtle total mercury content participates in the etiology of SR. Given that several toxins are known to affect both DNA methylation and/or mitochondrial DNA (mtDNA) copy number, we also probed for associations of these parameters to SR and mercury exposure. We measured the levels of each variable in malformed olive ridley sea turtle embryos (either with SR or other non-SR malformations) and embryos without malformations. Malformed embryos (with or without SR) showed higher mercury concentrations compared to normal embryos, while only embryos with SR showed higher levels of methylation compared to embryos without malformations and those with other malformations. Furthermore, we uncovered a positive correlation between mercury concentrations and DNA methylation in SR embryos. With respect to mtDNA copy number, no differences were detected across experimental groups. Because of sample size limitations, this study is an initial attempt to understand the association of environmental toxins (such as mercury) and epigenetic alterations (DNA methylation) in the etiology of SR in sea turtles.