The response of cultivated lymph node cells and blood neutrophils on soluble messengers produced by intact or toxically injured CBA mouse liver explants after in vitro 0.06 or 0.6 µM linoleyl-hydroxamic acid (LHA, lipoxygenase inhibitor) application was studied. The results showed that the action of LHA on intact liver resulted in stimulation of the lymph node cell proliferation and differentiation as well as of the neutrophil oxygen radical production and phagocytosis by liver supernatants. The tetrachlormetan-injured liver supernatants induced strong activation of both lymph node cell and neutrophil reactions. When LHA was added, injured liver more markedly activated lymph node cells, and selectively regulated neutrophil function: high oxygen radical production in neutrophils was reduced, but phagocytosis was kept up. These findings extend the support for a participation of lipoxygenase products in toxic hepatitis development through liver-mediated up-regulation of neutrophil reactions and limitation of lymph node cell activation. LHA as lipoxygenase blocker may be preferable for toxic hepatitis treatment as regards to favorable pattern of liver-mediated neutrophil reactions.