Aquatic Life Cycle Strategies: Survival in a variable environment. Occasional Publication of the Marine Biological Association 6

In a rapidly changing world it is essential that we should understand the factors controlling the sustainability of ecosystems. In aquatic ecosystems, both sensitivity and recoverability are influenced strongly by the life cycles of the organisms concerned. The response of individual species to change and their chances of survival in a variable environment can be affected dramatically by the timing and location of disturbances relative to their natural rhythms of fertilisation, dispersal and development. This book illustrates the wide range of issues that must be addressed to understand such relationships. Its purpose is to consider those aspects of life history that make aquatic organisms especially susceptible to (or adaptable to) changing environments -and hence to discuss links between impacts on individuals and the consequent effects on populations and communities.

High glucose decreases intracellular glutathione concentrations and upregulates inducible nitric oxide synthase gene expression in intestinal epithelial cells

Diabetes is associated with oxidative stress and increased levels of inflammatory cytokines. The aim of the study was to assess the effects of inflammatory cytokines and oxidative stress associated with raised glucose levels on inducible nitric oxide synthase (iNOS) promoter activity in intestinal epithelial cells. High glucose (25 mmol/l) conditions reduced glutathione (GSH) levels in the human intestinal epithelial cell line, DLD-1. Addition of the antioxidant alpha-lipoic acid resulted in the restoration of GSH levels to normal. Upregulation of basal iNOS promoter activity was observed when cells were incubated in high glucose alone. This effect was significantly reduced by the addition of the antioxidant, alpha-lipoic acid and completely blocked with inhibition of NFkappa B activity. Cytokine stimulation [interleukin-1 beta, tumor necrosis factor-alpha, interferon-gamma] induced iNOS promoter activity in all conditions and this was accompanied by an increase in nitric oxide (NO) production. Inhibition of NFkappa-B activity decreased but did not completely inhibit cytokine-induced iNOS promoter activity and subsequent NO production. In conclusion, high glucose-induced iNOS promoter activity is mediated in part through intracellular GSH and NFkappa-B.