Arruda Sandra Fernandes, Siqueira Egle Machado de Almeida, de Valência Fernando Fortes
Faculdade de Ciências da Saúde, Departamento de Nutrição, Campus Universitário Darcy Ribeiro, Universidade de Brasília, Asa Norte, Distrito Federal, Brazil.
Nutrition. 2009 Apr;25(4):472-8. doi: 10.1016/j.nut.2008.11.030. Epub 2009 Feb 12.
The interaction between vitamin A and iron status has been widely reported; however, the exact mechanism involved in this interaction has not been well characterized. The present study investigated the mechanism involved in tissue iron accumulation and changes in the oxidative status in vitamin A-deficient rats.
Rats were treated with a control diet, a vitamin A-deficient diet, or a vitamin A/iron-deficient diet for 57 d. The animals were sacrificed; the blood, liver, and spleen were collected for biochemical analysis. Analysis of variance or Mann-Whitney tests were used to compare groups and Pearson's or Spearman's tests to investigate the bivariate correlation.
Vitamin A deficiency increased liver hepcidin mRNA and iron spleen concentrations; however, iron deficiency in vitamin A-deficient rats deeply inhibits liver hepcidin mRNA expression and significantly increases divalent metal transporter-1 mRNA levels. Liver ferroportin and hereditary hemochromatosis gene mRNA levels did not change in either treatment. In the vitamin A-deficient groups, liver carbonyl protein increased, whereas catalase and glutathione S-transferase activities decreased, suggesting that vitamin A protects the liver against protein oxidation. A significant positive correlation was found between lipid oxidative damage and iron concentration in the liver and spleen (r = 0.611, P = 0.007; r = 0.558, P = 0.025, respectively).
These results suggest that vitamin A maintains iron homeostasis by the modulation of liver hepcidin expression. The increase of lipid peroxidation in vitamin A deficiency seems to be iron dependent, whereas protein oxidation is not.
维生素A与铁状态之间的相互作用已有广泛报道；然而，这种相互作用的确切机制尚未得到充分阐明。本研究调查了维生素A缺乏大鼠组织铁蓄积及氧化状态变化所涉及的机制。
大鼠分别用对照饮食、维生素A缺乏饮食或维生素A/铁缺乏饮食处理57天。处死动物，采集血液、肝脏和脾脏进行生化分析。采用方差分析或曼-惠特尼检验比较各组，并采用皮尔逊或斯皮尔曼检验研究双变量相关性。
维生素A缺乏会增加肝脏铁调素mRNA水平和脾脏铁浓度；然而，维生素A缺乏大鼠的缺铁会深度抑制肝脏铁调素mRNA表达，并显著增加二价金属转运体-1 mRNA水平。两种处理方式下肝脏铁转运蛋白和遗传性血色素沉着病基因mRNA水平均未改变。在维生素A缺乏组中，肝脏羰基蛋白增加，而过氧化氢酶和谷胱甘肽S-转移酶活性降低，表明维生素A可保护肝脏免受蛋白质氧化。肝脏和脾脏中脂质氧化损伤与铁浓度之间存在显著正相关（分别为r = 0.611，P = 0.007；r = 0.558，P = 0.025）。
这些结果表明，维生素A通过调节肝脏铁调素表达维持铁稳态。维生素A缺乏时脂质过氧化的增加似乎依赖于铁，而蛋白质氧化则不然。
