Parental exposure to toxicants can affect progeny health including when those exposures occur prior to conception. However most published preconception studies have involved exposures that result in loading of pollutants to gametes or toxic effects to parents which could indirectly affect germ cell or gamete health. Here we took advantage of the biology of Caenorhabditis elegans to carry out a preconception study in which we minimized the potential for maternal loading of toxicants and used an exposure paradigm that either did (high concentration) or did not (low concentration) significantly impact the health of the P0 generation. We hypothesized that preconception exposure to mitochondrial toxicants during germ cell and gamete development at levels not causing P0 toxicity would result in altered mitochondria and organismal health in offspring. In the P0 generation the high rotenone concentration altered growth mitochondrial respiration gene expression induction of the mitochondrial unfolded protein response and susceptibility to dopaminergic neurodegeneration induced by a chemical “rechallenge” later in life. However we observed minor or no effects in P0 at the low concentration. In high-exposure F1 offspring we observed altered embryo size larval developmental stage distribution spare respiratory capacity heat shock protein expression and dopaminergic neurodegeneration after a secondary rotenone challenge. The only effects observed in the F1 offspring of the low exposure were a 1.7% decrease in egg size (size later in development was normal) and moderate evidence of a slightly increased sensitivity to heat shock protein expression and dopaminergic neurodegeneration caused by a secondary later-in-life rotenone exposure.
