LOX-induced lipid peroxidation mechanism responsible for the detrimental effect of marine diatoms on zooplankton grazers.

Some marine diatoms negatively affect the reproduction of dominant zooplankton grazers such as copepods, thus compromising the transfer of energy through the marine food chains. In this paper, the metabolic mechanism that leads to diatom-induced toxicity is investigated in three bloom-forming microalgae. We show that copepod dysfunctions can be induced by highly reactive oxygen species (hROS) and a blended mixture of diatom products, including fatty acid hydroperoxides (FAHs); these compounds display teratogenic and proapoptotic properties. The process is triggered by the early onset of lipoxygenase activities that elicit the synthesis of species-specific products, the basic structures of which were established (1-20); these compounds boost oxidative stress by massive lipid peroxidation. Our study might explain past laboratory and field results showing how diatoms damage zooplankton grazers even in the absence of polyunsaturated aldehydes, a class of molecules that has been formerly implicated in mediating the toxic activity of diatoms on copepods.

Pulmonary microvascular injury from lipoxygenase infusion: comparison with endotoxemia.

We compared the response of the pulmonary microcirculation to a 5-hr infusion of soybean lipoxygenase with that seen after endotoxin. We monitored microvascular integrity using lung lymph flow QL and lymph/plasma (L/P) protein ratio in unanesthetized sheep. We noted a twofold to threefold increase in QL and a slight decrease in L/P ratio beginning about 1 hr after onset of the lipoxygenase infusion. Leukocyte count decreased significantly and lymph lysosomal enzyme activity increased. Pulmonary artery pressure initially increased from 16 to 31 mm Hg, then decreased to 25 mm Hg during continued infusion. Platelet count remained constant. Parameters returned to baseline several hours after infusion. This pulmonary vascular pressure and lymph flow response was very similar to that seen in the increased permeability phase of endotoxin. A decrease on the L/P ratio and a constant rather than a decreased platelet count were findings different from those seen after endotoxin.