Hydrogen sulfide (H2S) has dual actions in the human body as an endogenously produced signaling molecule and a toxic xenobiotic. It is a byproduct of several industries, including oil, petroleum and paper milling and natural forms of exposure are of concern for individuals living near landfills or volcanos. That hydrogen sulfide has potential for use as a chemical weapon is disconcerting. The gas is colorless and has a characteristic rotten egg odor. Acute H2S intoxication can lead to both short and long term neurological sequelae, including neurodegeneration, memory and motor impairment, however, the underlying mechanisms are still unknown. Our hypothesis is that neuroinflammation, characterized by an intense inflammatory response from activated glial cells, can cause cell death by invoking the production of many pro and anti-inflammatory cytokines. To test this hypothesis we used histopathology to visualize the affected tissue; then measured cytokines in the brain tissue and serum of mice exposed to H2S by inhalation. Results show increased glial fibrillary protein levels, indicating a recruitment of reactive astrocytes to the tissue, starting around day 3 post exposure. Understanding the basic mechanisms underlying neuroinflammation contributes to our long term objective of discovering countermeasures against and treatment of H2S induced neurodegeneration
