Low dose ionising radiation elicits MPTP comparable alterations in locomotor Function, oxidative balance and mitochondrial homeostasis in zebrafish embryos.

Prenatal exposure to environmental factors including low-dose ionising radiation and neurotoxins may disrupt the oxidant-antioxidant balance. Our aim was to assess the effects of exposure to low-dose ionising radiation (LDIR) and 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), which is a neurotoxin used to model Parkinson's disease (PD), on developing zebrafish embryos, focusing on the oxidant-antioxidant system and markers of mitochondrial damage associated with PD. Zebrafish embryos were divided into four groups: control, LDIR, MPTP, and LDIR combined with MPTP (LDIR + MPTP). A dental x-ray unit (60 kVp, 7 mA) was used for the exposures. The 0.08 s LDIR exposure was measured as 0.065 mGy using optically stimulated dosimeters. At the end of 72 h after fertilization, locomotor activities, acetylcholine esterase (AChE) activity, oxidative stress and antioxidant status were assessed. Expressions of genes associated with in PD as markers of mitochondrial damage (pink1, parkin, dj1 and lrrk2) were determined by RT-PCR. Developmental toxicity was observed in all exposure groups as evidenced by pericardial edema, yolk sac edema and spinal curvature. LDIR exposure in zebrafish embryos affected oxidative and mitochondrial stress markers, as well as locomotor activity and AChE as a marker of cognitive function at levels comparable to the MPTP exposure. Our study is the first to determine the effects of LDIR from a dental x-ray unit on the response to MPTP, and we aim to further elucidate the mechanism of these changes observed particularly in the LDIR + MPTP group.