Glutathione in blood cells decreases without DNA breaks after a simulated saturation dive to 250 msw.

Introduction: Saturation diving involves exposure to high pressure and elevated oxygen level. The impact of cellular defense systems like glutathione in protecting cells against oxidative DNA damage seems unclear. The aim of the present study was, therefore, to investigate whether diving conditions would affect blood cell glutathione and thus alter the mononuclear cells' (MNC) susceptibility to oxidative DNA damage. Methods: Eight subjects participated in a simulated saturation dive to 2.6 MPa (250 msw) lasting 19.3 d (0.8 d compression, 6.6 d bottom phase, 11.9 d decompression) breathing helium-oxygen with Po 2 ranging from 35 to 70 kPa (3.5-7.0 msw). Blood samples collected before compression and after decompression were analyzed for glutathione content and single-stranded DNA breaks. Results: The results demonstrate for the first time that a simulated saturation dive decreased glutathione content in peripheral blood cells (32% decrease in MNC), and that the decrease was most pronounced in the erythrocytes (45%). Remarkably, no single-stranded DNA breaks could be detected in the MNC despite the low glutathione level. Discussion: The results suggest that glutathione is a useful indicator of oxidative stress and that a low glutathione level represents no significant harm to the blood cells in the absence of other toxic agents. The lack of DNA strand breaks suggests that protection against oxidative DNA damage was mainly provided by mechanisms other than the glutathione system. Although previous investigations point to hyperoxia as the most plausible explanation for the present observations, the effect of high pressure cannot be excluded.