Data from: Metabolomic profiles of acute and chronic ambient hydrogen sulfide exposure in a mouse model

Hydrogen sulfide (H2S) is an environmental toxicant of health concern
following acute or chronic human exposures. Male 6-8 week-old C57BL/6J
mice were exposed by whole-body inhalation to 1000 ppm H2S for 45 min and
euthanized at 5 min and 72 h for acute exposure. For subchronic study,
mice were exposed to 5 ppm H2S 2 h/day, 5 days/week for 5 weeks. The
brainstem was removed for metabolomic analysis. The metabolomics analyses
consisted of three assays, (1) primary metabolism by GC-TOF MS, (2)
biogenic amines (hydrophilic compounds) by HILIC-MS/MS and (3) lipidomics
by RPLC-MS/MS. Metabolomics were performed in West Coast Metabolomics
Center, University of California at Davis, CA, USA. 348, 311, and 565
known metabolites were detected and analyzed by primary metabolism,
biogenic amines, and lipidomic metabolomics assays. 33, 19, and 46
metabolites were increased at 5 min and 72 h post acute H2S exposures and
subchronic ambient H2S exposures, respectively, compared to room air
control group. 22, 17, and 32 metabolites were decreased at 5 min and 72 h
post acute H2S exposures and subchronic ambient H2S exposures,
respectively, compared to room air control group. Acute H2S exposure
decreased excitatory neurotransmitters aspartate and glutamate
concentrations while the inhibitory neurotransmitter serotonin was
increased. Glutamate and serotonin were also decreased after ambient H2S
exposure. Branched-chain amino acids, fructose, and glucose were increased
by acute H2S exposure. In ambient H2S exposure, glucose was decreased
while MUFAs, PUFAs, inosine, and hypoxanthine were increased.
Collectively, these results provide important mechanistic clues of acute
and subchronic ambient H2S poisonings and show that H2S alters
neurotransmission homeostasis.