Toxicity of oxidized beta-carotene to cultured human cells.

Carotenoids are effective antioxidants in vitro, but they are also susceptible to autoxidation, which generates volatile and biologically active aldehydes and ketones. In a previous study, we showed that autoxidized beta-carotene inhibits Na+-K+-ATPase activity more effectively than aldehydic products derived from lipid peroxidation, such as 4-hydroxynonenal. In this study, we compared mitochondrial dysfunction in cultured human K562 erythroleukaemic and 28 SV4 retinal pigment epithelium (RPE) cells in response to the degradation products of beta-carotene autoxidation using the MTT assay.

Electrospray tandem mass spectrometric analysis of zeaxanthin and its oxidation products.

Carotenoids have been implicated in protection of the eye from light-mediated photo-toxicity caused by free radicals. Under conditions of normal oxidative stress the carotenoids serve as protective antioxidants; however, when the oxidative stress exceeds the antioxidant capacity, carotenoids can be oxidized into numerous cleavage products. The determination and identification of oxidized carotenoids in biological samples remains a major challenge due to the small sample size and low stability of these compounds.

Oxidation of carotenoids by heat and tobacco smoke.

The stability to autoxidation of the polar carotenoids, lutein and zeaxanthin, was compared to that of the less polar carotenoids, beta-carotene and lycopene at physiologically or pathophysiologically relevant concentrations of 2 and 6 microM, after exposure to heat or cigarette smoke. Three methodological approaches were used: 1) Carotenoids dissolved in solvents with different polarities were incubated at 37 and 80 degrees C for different times. 2) Human plasma samples were subjected to the same temperature conditions.

Bcl-2 overexpression increases survival in human retinal pigment epithelial cells exposed to H(2)O(2).

The integrity of the retinal pigment epithelium, especially that of the macula is essential for the preservation of vision into old age. The chronic exposure to sunlight and peroxidized lipids from phagocytized photoreceptor outer segments imposes a high level of oxidative stress on the retinal tissues, which increases with age as antioxidant protection declines and therefore could accelerate apoptosis. Bcl-2 known to facilitate mitochondrial DNA repair and cellular survival in other tissues was overexpressed in a single clone of human retinal pigment epithelium cells after stable transfection with humanbcl-2 in rhoSFV-neoexpression factor.