Metabolomic analysis of the effects of motorcycle exhaust on rat testes and liver

Motorcycles are one of the primary means of transportation in many Asian metropolitan areas. Exposure to motorcycle exhaust (ME) has been shown to cause male reproductive toxicity in a rat inhalation model. In the present study, the molecular mechanisms underlying ME-induced male reproductive toxicity were examined in a rat model using nuclear magnetic resonance (NMR)-based metabolomics. Rats were treated with 1:10-diluted ME for 1 hour in the morning and 1 hour in the afternoon, daily, via head-nose-only exposure chambers, for a period of four weeks. Half of the ME-exposed rats were co-treated with vitamin E to examine its protective effects. Both hydrophilic and hydrophobic metabolites from the testes and liver were extracted for ¹H and J-resolved NMR analyses. The obtained NMR spectra were converted into series of spectral binned areas and subjected to orthogonal projections to latent structure-discriminant analyses. Decreased spermatid counts and elevated levels of betaine in the testes of rats in the ME-treated group were partially attenuated by vitamin E co-treatment. Although it was not statistically significant, we observed a consistent trend of partial reversal of the elevated levels of alanine, glycine, leucine, tyrosine, and valine in the testes of rats in the ME-treated group due to vitamin E co-treatment. Decreases in testicular ethanolamine and inositol were only significant in the group co-treated with ME and vitamin E. The testicular toxicity of ME may be due to alterations in lipid- and energy-related metabolism. We conclude that ME generates greater metabolic responses in the testes than in the liver. Treatment with vitamin E can partially reverse the molecular events in the testes.