Growth inhibitory effects of 15-lipoxygenase-1 and 15-lipoxygenase-2 (15-LOX-1 and LOX-2) metabolites and the underlying mechanisms were studied on chronic myeloid leukemia cell line (K-562). In this study, the loss of lipids potentially increased the availability for enzyme-independent lipid peroxidation, leading to cell fragility and death.
Antioxidant enzymes activities were also increased in sonoporated Jurkat cells compared with the control. Levels of enzyme-independent oxidized products (F 2-isoprostanes, F 3-isoprostanes, 7-ketocholesterol) were elevated by sonoporation compared with the control, whereas enzyme-dependent oxidized products (5(S)-, 9(S)-, 12(S)-, 15(S)- and 20-HETE and 27-hydroxycholesterol) were not altered. Sonoporation suppressed cholesterol concentration and arachidonic, eicosapentaenoic and docosahexaenoic acids in the Jurkat cells. A reduction in cell viability and an induction of apoptosis of Jurkat cells were found 4 h and 24 h post-sonoporation, respectively. In this study, cell viability and the generation of specific oxidized lipid products were assessed in Jurkat cells before and after sonoporation. Low frequency ultrasound is used to trigger the cavitation of microbubbles to puncture the cell membrane, and during this process, lipid metabolism becomes disrupted. Sonoporation is a developing technique used in drug delivery for cancer cells. Unlike the hydro(pero)xides, the terminal products of the arachidonate cascade (i.e., leukotrienes, prostaglandins and thromboxane) were not cytotoxic.
On the other hand, lipoxygenase products evoked an immediate and sustained rise in cytoplasmic calcium (within seconds), followed by mitochondrial uncoupling (within hours). PCD elicited by lipoxygenase products was independent of intracellular glutathione concentration, and did not require mRNA transcription or protein synthesis. After 24 h, K562 and CHP100 cells showed 2.5- to 3.5-fold more apoptotic bodies than the untreated controls. The hydroperoxides generated by 5-, 12-, or 15-lipoxygenases from linoleate, linolenate, or arachidonate, and the corresponding hydroxides, were able to induce PCD in both cell types, in a concentration- and time-dependent manner. Erythroleukemia K562 and neuroblastoma CHP100 cells were used, because they showed high basal activity of lipoxygenase. Changes in organic content with depth are used to show that contemporary sediment accumulation rates at some locations have reduced the ability of benthic fauna to rework sediment.We investigated the ability of different hydroperoxides generated by lipoxygenase isozymes to induce programmed cell death (PCD) in human cells. Gross and net sedimentation rates were of a similar order of magnitude. During flood events, wind direction, speed and duration have a significant influence on sediment deposition. There are distinctly seasonal patterns of low summer and high winter sediment accumulation rates, although there are individual peaks related to flood events. Sediment accumulation rates of up to 60 mm yr-1 were recorded with a marked, and sustained, increase occurring in the early 1950's as a result of anthropogenic activity (dumping of dredged material and aggregate extraction). Sediment traps were deployed adjacent to core sites for a period of 15 months. Three cores were analysed by 137Cs, one producing an annual to decadal record of sediment accumulation, the first recorded examples from marine sediments in New Zealand. Recent sediment accumulation in Wellington Harbour was recorded by core and sediment trap data.
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