Abstract

Virgin coconut oil (VCO), prepared from fresh coconut kernel without any chemical refining, is an emerging functional food. The pharmacological benefits of VCO are believed to be due to the natural combination of phenolics. Although cell culture studies have demonstrated the antioxidant activity of VCO under different oxidative stress conditions, a valid in vivo demonstration of the antioxidant activity of VCO is yet to come. Sodium fluoride (NaF), an environmental pollutant, is widely used to induce oxidative stress in cell culture models and rodents to test the antioxidant potential of several compounds. Herein, VCO and its polyphenolic (VCOP) and non-phenolic oil fraction (VCOF) were individually tested in fluoride-exposed normal intestinal cells (IEC-6) and mice to address their contribution to the documented antioxidant potential. It was found that pretreatment of VCOP (40 µg/mL) was effective in mitigating the fluoride-induced cell death when compared to VCO (200 µg/mL) and VCOF (160 µg/mL). Further, exposure to fluoride (10 mM), increased the intracellular ROS measured based on the dichlorofluorescein (DCF) fluorescence, and this, in turn, was significantly reduced when the cells were supplemented with VCOP. Oral administration of VCO (2 mL/kg bwt) reversed the drop in the hepatic catalase and SOD activities to near normal with a minimal level of lipid peroxidation in fluoride intoxicated mice. However, VCOP and VCOF were less effective in lowering the fluoride-induced increase in hepatic oxidative stress markers. It is reasoned that the oil components of VCO complement the natural antioxidant molecules resulting in an overall increase in their bioavailability.

摘要

初榨椰子油（VCO）由新鲜椰子仁未经任何化学精炼制成，是一种新兴的功能性食品。VCO 的药理益处被认为是由于酚类物质的天然组合。尽管细胞培养研究已经证明了 VCO 在不同氧化应激条件下的抗氧化活性，但在体内有效VCO 的抗氧化活性的证明尚未到来。氟化钠 (NaF) 是一种环境污染物，广泛用于在细胞培养模型和啮齿动物中诱导氧化应激，以测试几种化合物的抗氧化潜力。在这里，VCO 及其多酚 (VCOP) 和非酚油馏分 (VCOF) 在暴露于氟化物的正常肠细胞 (IEC-6) 和小鼠中进行了单独测试，以解决它们对记录的抗氧化潜力的贡献。发现与 VCO (200 µg/mL) 和 VCOF (160 µg/mL) 相比，VCOP (40 µg/mL) 的预处理在减轻氟化物诱导的细胞死亡方面是有效的。此外，暴露于氟化物 (10 mM) 会增加基于二氯荧光素 (DCF) 荧光测量的细胞内 ROS，而这反过来，当细胞补充 VCOP 时显着降低。口服 VCO (2 mL/kg bwt) 可将肝过氧化氢酶和 SOD 活性的下降逆转至接近正常水平，并且在氟化物中毒的小鼠中脂质过氧化水平最低。然而，VCOP 和 VCOF 在降低氟化物诱导的肝氧化应激标志物增加方面效果较差。据推测，VCO 的油成分补充了天然抗氧化剂分子，从而整体提高了它们的生物利用度。