β-Carotene and lutein protect HepG2 human liver cells against oxidant- induced damage

Abstract

Numerous epidemiological studies support a strong inverse relationship between consumption of carotenoid-rich fruits and vegetables and the incidence of some degenerative diseases. One proposed mechanism of protection by carotenoids centers on their putative ant/oxidant activity, although direct evidence in support of this contention is limited at the cellular level. The ant/oxidant potential of β-carotene (BC) and lutein (LUT), carotenoids with or without provitamin A activity, respectively, was evaluated using the human liver cell line HepG2. Pilot studies showed that a 90-min exposure of confluent cultures to 500 μmol/L tert-butylhydroperoxide (TBHP) at 37°C significantly (P < 0.05) increased lipid peroxidation and cellular leakage of lactate dehydrogenase (LDH), and decreased the uptake of 3H-α-aminoisobutyric acid and 3H-2-deoxyglucose. Protein synthesis, mitochondrial activity and glucose oxidation were not affected by TBHP treatment, suggesting that the plasma membrane was the primary site of TBHP- induced damage. Overnight incubation of cultures with ≤ 1 μmol/L dl-α- tocopherol protected cells against oxidant-induced changes. In parallel studies, overnight incubation of HepG2 in medium containing micelies with either BC or LUT (final concentrations of 1.1 and 10.9 μmol/L, respectively), the cell content of the carotenoids increased from <0.04 to 0.32 and 3.39 nmol/mg protein, respectively. Carotenoid-loaded cells were partially or completely protected against oxidant-induced changes in lipid peroxidation, LDH release and amino acid and deoxyglucose transport. These data demonstrate that BC and LUT or their metabolites protect HepG2 cells against oxidant-induced damage and that the protective effect is independent of provitamin A activity.

Publication Title

Journal of Nutrition

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