Effect of fenofibrate on kidney function: a 6-week randomized crossover trial in healthy people.

Background: Fenofibrate was associated with increases in serum creatinine concentrations. The effect of short-term fenofibrate treatment on kidney function was investigated in subjects with normal kidney function.

Study Design: Double-blind, crossover, placebo-controlled.

Determination of aminothiols in body fluids, cells, and tissues by capillary electrophoresis.

Oxidative stress is present in cardiovascular diseases and hyperhomocysteinemia, an independent risk factor for these diseases. It may play a role by inducing production of oxygen free radicals. Reduced glutathione is the most abundant intracellular low-molecular-weight thiol and plays an essential role in protecting cells from toxic species.

Analysis of tryptophan and tyrosine in cerebrospinal fluid by capillary electrophoresis and "ball lens" UV-pulsed laser-induced fluorescence detection.

For the purpose of this study, we used a "ball lens" UV laser-induced fluorescence (LIF) detector comprising a pulsed laser and a collinear optical arrangement. The fluorescence signal is induced by a pulsed laser and detected by a photomultiplier tube. When coupling the high-frequency pulsed laser to the LIF detector we used, the electronics which is designed for continuous wavelength (CW) lasers, "viewed" the laser as a continuous source.

Methods for homocysteine analysis and biological relevance of the results.

It is now widely accepted that increased total plasma homocysteine (tHcy) is a risk factor for cardiovascular disease. Hyperhomocysteinemia can be caused by impaired enzyme function as a result of genetic mutation or vitamin B (B(2), B(6), B(9), B(12)) deficiency. A lot of methods are now available for tHcy determination.

Fenofibrate induces a selective increase of protein-bound homocysteine in rodents: a PPARalpha-mediated effect.

Elevated levels of plasma homocysteine (Hcy) are associated with increased risk of cardiovascular disease though it is uncertain whether increases in Hcy represent a cause or a consequence of the disease process. Plasma Hcy exists in reduced, free oxidized, and protein-bound forms, that together comprise total Hcy (tHcy). Free reduced Hcy is thought to be the atherogenic, though minor, sub-fraction of tHcy.