H 2 S induces lysosomal rupture in erythrocytes from an H 2 S‐tolerant marine polychaete

H 2 S and H 2 O 2 can each react with divalent metals to produce free radicals through Fenton‐type reactions. Lysosomes, which accumulate iron, are ruptured by H 2 O 2 exposure in cultured mammalian cells, leading to cell death, and this effect is minimized by antioxidants. Many marine invertebrates are exposed to potentially toxic concentrations of H 2 S in their environment, but it is unknown whether this can result in loss of lysosomes. We tested whether H 2 S can cause lysosomal rupture in cells from a H 2 S‐tolerant marine invertebrate in vitro , and whether this effect can be minimized by antioxidants. We exposed erythrocytes from the marine mudflat polychaete Glycera dibranchiata to 0.01‐1 mM H 2 O 2 for 1 h or 0.03‐1% H 2 S for 2 h in vitro , after which we used LysoTracker Red (LTR) and acridine orange to quantify lysosome number and staining intensity. Both H 2 O 2 and H 2 S exposure decreased the integrated intensity of LTR by up to 63% (p=0.0051) and 76% (p<0.0001), respectively, and lysosomal area by 61% (p=0.0150) and 81% (p<0.0001), respectively. However, the effects of H 2 S were not reduced by the antioxidants glutathione ethyl ester, N‐acetylcysteine or hypotaurine. Therefore, H 2 S exposure causes loss of lysosomes similar to that of H 2 O 2 exposure, even in an animal adapted to H 2 S, but it remains unclear whether this effect is via oxidative damage.