Dietary glycine inhibits activation of nuclear factor kappa B and preventsliver injury in hemorrhagic shock in the rat

We investigated the effects of a glycine-containing diet (5%) on liver inju ry caused by hemorrhagic shock and resuscitation in rats. Anesthetized rats were bled to a mean arterial blood pressure of 35-40 min Hg for 1 h and th en resuscitated with 60% of shed blood and lactated Ringer's solution. Feed ing the rats glycine significantly reduced mortality, the elevation of plas ma transaminase levels and hepatic necrosis. The increase in plasma TNF alp ha and nitric oxide (NO) was also blunted by glycine feeding. Hemorrhagic s hock resulted in oxidative stress (significant elevations in TBARS and in t he oxidized/reduced glutathione ratio) and was accompanied by a reduced act ivity of the antioxidant enzymes Mn- and Cu,Zn-superoxide dismutase, glutat hione peroxidase and catalase, overexpression of inducible NO synthase (iNO S), and activation of nuclear factor kappa B (NF-kappaB). Glycine ameliorat ed oxidative stress and the impairment in antioxidant enzyme activities, in hibited NF-kappaB activation, and prevented expression of iNOS. Dietary gly cine blocks activation of different mediators involved in the pathophysiolo gy of liver injury after shock. (C) 2001 Elsevier Science Inc.