PSC 833 can be administered in combination with etoposide with acceptable toxicity. The recommended continuous infusion dose of PSC 833 for this schedule is 10 mg/kg/d over 5 days. PSC 833 results in an increase in etoposide exposure and etoposide doses should be reduced in patients receiving PSC 833.
The death of macrophages contributes to atheroma formation. Oxidation renders low-density lipoprotein (LDL) cytotoxic to human monocyte-macrophages. Lipoprotein-associated phospholipase A 2 (Lp-PLA 2 ), also termed platelet-activating factor acetylhydrolase, hydrolyses oxidised phospholipids. Inhibition of Lp-PLA 2 by diisopropyl fluorophosphate or Pefabloc (broad-spectrum serine esterase/protease inhibitors), or SB222657 (a specific inhibitor of Lp-PLA 2 ) did not prevent LDL oxidation, but diminished the ensuing toxicity and apoptosis induction when the LDL was oxidised, and inhibited the rise in lysophosphatidylcholine levels that occurred in the inhibitors' absence. Hydrolysis products of oxidised phospholipids thus account for over a third of the cytotoxic and apoptosisinducing effects of oxidised LDL on macrophages. ß
Background and purpose: We have recently shown that the phytocannabinoid D 9 -tetrahydrocannabivarin (D 9 -THCV) and the CB 1 receptor antagonist AM251 increase inhibitory neurotransmission in mouse cerebellum and also exhibit anticonvulsant activity in a rat piriform cortical (PC) model of epilepsy.
Human monocyte-macrophages were incubated for 24 h in Ham's F-10 medium with human low-density lipoprotein (LDL) in the presence or absence of ß-carotene, canthaxanthin or zeaxanthin, at final concentrations of 2.5, 12.5 and 25 mg/1. LDL oxidation, measured by agarose gel electrophoresis, the thiobarbituric acid assay and gas chromatography, was inhibited by each of the carotenoids in a concentration-dependent manner. Canthaxanthin was more effective when incorporated into LDL before addition to the cultures whereas ß-carotene and zeaxanthin were more effective when added simultaneously with LDL. The results suggest that dietary carotenoids might help slow atherosclerosis progression.
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