Department of Toxicology, Medical University of Bialystok, Adama Mickiewicza 2C street, 15-222 Bialystok, Poland.
Department of Medical Chemistry, Medical University of Bialystok, Adama Mickiewicza 2A, 15-222 Bialystok, Poland.
Nutrients. 2019 Mar 31;11(4):758. doi: 10.3390/nu11040758.
It was investigated, using a female rat model of low and moderate exposure of human to cadmium (Cd, 1 and 5 mg Cd/kg diet for 3⁻24 months), whether a polyphenol-rich 0.1% aqueous extract from L. berries (AE) may prevent Cd-induced lipid peroxidation and oxidative modifications of proteins and deoxyribonucleic acid (DNA) in the liver. For this purpose, markers of lipid peroxidation (lipid peroxides and 8-isoprostane) and oxidative injury of proteins (protein carbonyl groups and 3-nitrotyrosine) and DNA (8-hydroxy-2'-deoxyguanosine) were measured in this organ. The expression of metallothionein 1 (MT1) and metallothionein 2 (MT2) genes was estimated for a better explanation of the possible mechanisms of protective action of AE against Cd hepatotoxicity. The low and moderate treatment with Cd induced lipid peroxidation and oxidatively modified proteins and DNA, as well as enhanced the expression of MT1 and MT2 in the liver, whereas the co-administration of AE completely prevented almost all of these effects. The results allow us to conclude that the consumption of aronia products under exposure to Cd may offer protection against oxidative injury of the main cellular macromolecules in the liver, including especially lipid peroxidation, and in this way prevent damage to this organ.
采用雌性大鼠模型，研究了人类低、中水平镉暴露（1 和 5mgCd/kg 饮食，暴露时间为 3-24 个月），多酚含量丰富的蓝莓 0.1%水提物（AE）是否可以预防镉引起的肝脂质过氧化、蛋白质氧化修饰和脱氧核糖核酸（DNA）损伤。为此，在该器官中测量了脂质过氧化的标志物（脂质过氧化物和 8-异前列腺素）和蛋白质氧化损伤的标志物（蛋白质羰基和 3-硝基酪氨酸）以及 DNA 损伤的标志物（8-羟基-2'-脱氧鸟苷）。为了更好地解释 AE 对镉肝毒性的保护作用的可能机制，还估计了金属硫蛋白 1（MT1）和金属硫蛋白 2（MT2）基因的表达。低、中水平的镉处理诱导了肝脂质过氧化、蛋白质氧化修饰和 DNA 损伤，同时增强了 MT1 和 MT2 在肝中的表达，而 AE 的共同给药几乎完全阻止了所有这些效应。结果表明，在接触镉的情况下，摄入蓝莓产品可能提供针对肝内主要细胞大分子的氧化损伤的保护，包括特别针对脂质过氧化，从而防止该器官受损。
