| Atherosclerosis (AS) is one of the most serious diseases in human, and the cholesterol oxidation products (Ch-Ox) are currently considered as a key atherogenic factor in its pathogenesis. The researches on the cytotoxicity of Ch-Ox and its mechanism, the prevention and cure of AS are one of the frontier fields in human health.In this paper, the effect of Triol on oxidative impairment of isolated mouse liver mitochondria and the probable mechanism were investigated. The main results are as follows:1. The effect of Cholestane-3β, 5α, 6β-triol(Triol) on lipid peroxidation, membrane protein oxidation, H2O2 generation, transmembrane potential, release of cytochorme c of isolated mouse liver mitochondria were studied. The results indicated that Triol induced lipid peroxidation and membrane protein oxidation, decrease of transmembrane potential, and increase of H2O2 generation and cytochorme C release.2. To further investigate the mechanism, the effects of Triol on the activity of three enzymes in mitochondria respiratory chain were studied. The results suggested that complex I and II enzyme activity increased, while complex III enzyme activity did not change significantly as Triol applied to intact mitochondria. Furthermore, complex I and III enzyme activity decreased, and complex II enzyme activity increased as Triol applied to broken mitochondria.3. The effect of Triol on membrane protein secondary structure of human ghost was studied by Attenuated Total Reflection-Fourier Transform Infrared Spectroscopy (ATR- FTIR). The results showed thatα-helix increased dose- and time-dependently, andβ-sheet decreased at high concentration of Triol but increased as time prolonged, and random as well as turns reduced dose- and time-dependently.
|
PDF Full Text Request