How two species interact, whether the host benefits or is degraded by the microbe depends mainly on two factors: the effectiveness of the defense reaction of the host and the pathogenicity of the microorganism. In this study we investigated the interaction of the most abundant seagrass in the northern hemisphere, Zostera marina, with the endophytic protist Labyrinthula zosterae, which caused the world’s largest reported seagrass die-off event. Seagrasses form one of the most valuable coastal ecosystems on earth. They are marine flowering plants, which form huge meadows, providing food, shelter and settlement substrate for many organisms. Being the foundation species of one of the most productive ecosystems, they sequester 15% of the total marine consumed CO2 and represent thereby an important sink and storage of atmospheric CO2. Seagrass meadows contribute to coastal protection. Seagrasses are sensitive to reduced light availability due to eutrophication or increasing water turbidity. Since anthropogenic impact on this sensitive ecosystem is still increasing, seagrass populations are declining worldwide. The development of lesions covering significant parts of the leaf was correlated with a significant increase in growth rate of the uninoculated younger leaves of the same shoot. Similar plant – endophyte interactions that lead to increased growth and shoot production and ultimately result in enhanced survival of the host as a consequence of infection are known from many terrestrial grass species. The mechanisms underlying this effect are for example enhanced nutrient use efficiency for nitrogen and phosphorus. Endophyte-infected terrestrial grasses also exhibit fundamental changes in their secondary metabolites including a range of alkaloids and phenolic compounds.Phenols produced by endophyte-infected grasses can not only be a reaction upon infection but for example be released through root exudates leading to an increase in P availability. Urolithiasis is a complex disease characterized by the formation of stones in the urinary tract. Accumulating lines of R428 evidence suggest that renal tubular cell injury and fixed crystal particles could be GSK1363089 implicated in the pathogenesis of urolithiasis. Others have postulated that excessive excretion of urinary oxalate could cause substantial damage to the renal epithelium. Others have reported that oxalate generates excessive free radicals leading to renal epithelial cell injury and membrane lipid peroxidation, which in turn favors urolithogenesis. Exposure to oxalate, a major component of kidney stones, elicits a cascade of responses in renal epithelial cells that often leads to cell injury or death. Numerous studies have suggested that oxalate toxicity is accompanied by the generation of reactive oxygen species in renal cell cultures. Oxalate exposure also imposes oxidative stress on renal cells by stimulating accumulation of lipid peroxides while decreasing the availability of other cellular antioxidants. Intracellular and intra-mitochondrial antioxidants prevent cellular damage due to endogenous ROS, although conditions that increase ROS generation or diminish antioxidant availability could increase intracellular accumulation of ROS. Accumulating body of evidence suggests that mitochondria represent an important source of ROS, produced in renal cells following exposure to oxalate.