Meeting Abstract
Cellular hydrogen sulfide (H2S) is a gasotransmitter (like nitric oxide) required for life-extension by dietary restriction in mice. H2S protects vasculature in mammals. In nematodes, H2S exposure increases thermotolerance and lifespan. In insects, the production of H2S by Drosophila fed life-extending, low-methionine diets is greater than production on full diets. Together, this suggests increased H2S production is salubrious for invertebrates. Nonetheless, insects are often said to be ‘weak producers’. Here, we provide preliminary evidence for inhibition of H2S production by lysates of grasshopper fat body. Fat body is analogous to liver, the most strongly producing tissue in mice. We tested production of H2S using an enzyme activity assay. Lysates were incubated with cysteine and vitamin B6; produced H2S was detected using lead acetate, which in the presence of H2S makes the brown precipitate lead sulfide. Surprisingly, higher concentrations (50 ul, median of ~8 mg protein) of fat body lysate consistently produced less H2S than did lower concentrations (0.69 mg protein). Decreasing the protein amount below 0.69 mg reduced H2S production in a dose-dependent fashion. We next tested whether fat body lysate would inhibit production of H2S by homogenates of mouse liver. Indeed, increasing concentrations of fat body lysate tended to decrease H2S production by mouse liver homogenate (n=19; P=0.075). In contrast to this inhibition by grasshopper fat body, lysates of mealworms did not inhibit production of H2S by mouse liver homogenate. These data suggest that a component of the lysate of grasshopper fat body, when present at higher concentrations, inhibits enzymatic production of H2S by liver homogenates.
