ABSTRACT
A suplementação de ß-caroteno em fumantes e alcoólatras pode promover efeitos indesejáveis, manifestando a característica pró-oxidante deste carotenóide. Sabendo que o fígado é principal órgão de armazenamento de vitamina A e ß-caroteno, e local de oxidação do etanol, o presente estudo buscou investigar no fígado de ratos, a influência da suplementação de ß-caroteno isolado ou associado ao etanol, sobre o metabolismo celular, danos no DNA, proliferação celular e função da proteína p53. Os ratos receberam dietas líquidas contendo ß-caroteno (24mg/L dieta) com (GAB) ou sem (GBC) a adição de etanol (36 porcento da calorias totais da dieta) e dieta líquida normal (isenta de ß-caroteno e etanol) (GDN), durante seis semanas de período experimental...
ß-carotene, when supplemented in smokers and alcohol drinkers may act as prooxidant, resulting in undesirable effects. The liver is the ß-carotene and vitamin A main storage organ and where ethanol oxidation takes place. This study investigated in rats' liver, the influence of ß-carotene supplementation either alone or associated with ethanol in cellular metabolism, DNA damage, cellular proliferation and p53 protein function. Three groups of 12 rats received liquid diets containing ß-carotene (24mg/L diet) with (BAG) or without (CBG) ethanol (36% of total energy intake). Control animals received liquid diet free of ethanol and ß-carotene (NDG). After 6 weeks the animals were sacrificed for hepatic and plasma concentrations of ß-carotene, retinol, palmitate retinyl, steatosis, GSH and TBARS, DNA damage, PCNA and p53 expression were evaluated in the liver. Differences were significant for hepatic (BAG: 2.49 ± 0.25; CBG: 4.22 ± 0.24; NDG: 2.83 ± 0.21 mg/g) and plasmatic (BAG: 1.42 ± 0.12; CBG: 0.69 ± 0.06; NDG: 2,37 ± 0,28mmol/L) retinol and hepatic palmitate retinyl (BAG: 40.87 ± 3.98; CBG: 83.72 ± 6.00; NDG: 46.33 ± 3.60), steatosis (BAG: 2.30 ± 0.21; CBG: 1.00 ± 0.00; NDG: 1.00 ± 0.00), DNA damage (BAG: 285.90 ± 15.20; CBG: 273.83 ± 13.39; NDG: 138.00 ±4.04 DNA damages/100 hepatocytes) and PCNA expression (BAG: 7.12 ± 1.46; CBG: 1.47 ± 0.27; NDG: 2.04 ± 0.31) among the groups (p<0.05). Hepatic and plasmatic concentrations of ßcarotene, TBARS and GSH were not statistically different. p53 staining was not detected in any group. This suggests that ß-carotene alone or with ethanol association does not influence lipid peroxidation and p53 expression. ß-carotene+ethanol caused metabolic alteration, steatosis, DNA damage and cellular proliferation in hepatocytes. Furthermore, supplementation with ß-carotene alone had genotoxic effects in the liver.