Normolipidic diet containing deep-fried saturated and unsaturated fatty acids rich edible oils promotes metabolic dysregulation and inflammatory microenvironment in Wistar rats.

Deleterious health impacts of high dietary intake of deep-fried edible oils have been reported however, their health impacts at normal dietary levels are yet to be evaluated. This study investigated the influence of prolonged consumption of thermally oxidised long-chain saturated and unsaturated edible oils on metabolic dysregulation and inflammation. The thermally oxidised oils used in the study possess higher p-anisidine values and free fatty acid contents compared to unoxidised oils. Fourier transform infrared spectroscopy and fatty acid methyl ester analysis confirmed the presence of free fatty acids, hydroperoxides, and aldehydes, formed during thermal oxidation. The study analysed the effects of dietary intake of 5% sunflower oil, palm oil, and their thermally-oxidised forms in male Wistar rats for six months. Unoxidised and thermally oxidised palm oil-fed animals experienced metabolic syndrome with obesity-associated inflammatory changes. However, sunflower oil-fed animals exhibited increased inflammation, as evidenced by enhanced C-reactive protein, IL-6, and lipoprotein-associated phospholipase A2 activity and hepatosteatosis condition. This study indicates that prolonged consumption of thermally oxidised oil leads to the dysregulation of carbohydrate and lipid metabolism andpromotes inflammatory microenvironment in Wistar rats that may contribute to metabolic syndrome associated with obesity and hepatic steatosis.

Hot-processed virgin coconut oil abrogates cisplatin-induced nephrotoxicity by restoring redox balance in rats compared to fermentation-processed virgin coconut oil.

Virgin coconut oil (VCO) is a functional food oil prepared from fresh coconut kernel either by hot-processed (HPVCO) or fermentation-processed (FPVCO). The FPVCO has been widely explored for its pharmacological efficacy; while HPVCO, which has traditional uses, is less explored. The present study compared the phenolic content and nephroprotective effect of both these oils in male Wistar rats. In vitro antioxidant activity was estimated in terms of 2,2-diphenyl-1-picrylhydrazyl (DPPH) radical scavenging, ferric reducing antioxidant power and ex vivo lipid peroxidation inhibition. In in vivo models, the rats were pretreated orally with of FPVCO or HPVCO (doses 2 and 4 mL/kg) for seven days and nephrotoxicity was induced by the single intraperitoneal injection of cisplatin (10 mg/kg). The results indicated significantly higher polyphenol content in HPVCO (400.3 ± 5.8 µg/mL) than that of FPVCO (255.5 ± 5.8 µg/mL). Corroborating with the increased levels of polyphenols, the in vitro antioxidant potential was significantly higher in the HPVCO. Further, pretreatment with these VCO preparations protected the rats against the cisplatin-induced nephrotoxicity, with higher extent by HPVCO. The renal function markers like urea, creatinine and total bilirubin were significantly reduced (p < 0.05) with HPVCO pretreatment. Apart from the nephroprotective effects, HPVCO also abrogated the cisplatin-induced myelosuppression and hepatotoxicity. The restoration of hepato-renal function by the pretreatment of HPVCO was well corroborated with the improvement in functional antioxidants and subsequent reduction in renal lipid peroxidation. Supporting these observations, renal histology revealed reduced glomerular/tubular congestion and necrosis. Thus, the study concludes that HPVCO may be better functional food than FPVCO.

Virgin coconut oil complements with its polyphenol components mitigate sodium fluoride toxicity in vitro and in vivo.

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.

Variations in natural polyphenols determine the anti-inflammatory potential of virgin coconut oils.

Virgin coconut oil (VCO), an edible oil prepared from fresh coconut kernel by natural or mechanical means without undergoing chemical refining, has been in the limelight of research as functional food oil. The phenolic components in VCO have been accredited with these pharmacological benefits. The present study compared the phenolic constituents of freshly prepared fermentation processed (FVCO) and hot-pressed VCO (HVCO) and their anti-inflammatory efficacies. The biochemical analysis documented quantitative variation in the phenolic content, being higher in HVCO than FVCO (40.03 ± 5.8 µg and 25.55 ± 5.8 µg/mL of oil, respectively). In vitro studies observed nitric oxide radical scavenging efficacy (IC50 value of 14.84 ± 0.81 µg/mL) for HVCO polyphenols, which shows higher inhibition efficacy than FVCO (29.41 ± 1.7 µg/mL). In dextran and formalin mediated acute and chronic inflammation in mice, HVCO displayed more protective efficacy (40.5 and 46.4% inhibition) than FVCO (33.3 and 43.8% inhibition), which is similar to the standard diclofenac (55.6 and 59.8% inhibition). The study, thus, concludes that compared to FVCO, HVCO is a more active anti-inflammatory agent. PRACTICAL APPLICATION: Virgin coconut oil, a widely used edible oil in South Asian countries, has been shown to have health benefits possibly exerted by the natural phenolics it contains. However, different modes of preparations of VCO determine the phenolic combinations and efficacy as well. Our study compared two different VCO preparations and suggests that the VCO prepared by the traditional way (HVCO) is pharmacologically potent than that prepared by simple fermentation process (FVCO) in reducing inflammation. The efficacy is attributed to the variations in phenolic profile revealed by LC-MS analysis. Hence, the current study suggests HVCO as a potential food supplement that can reduce the incidence of degenerative diseases.

Curcumin Enriched VCO Protects against 7,12-Dimethyl Benz[a] Anthracene-Induced Skin Papilloma in Mice.

Virgin coconut oil (VCO) and turmeric are traditionally being used in Indian cuisine systems; VCO is a natural combination of medium-chain triglyceride and polyphenols with established pharmacological potential. Curcumin isolated from turmeric is renowned for its anticancer properties, however, with limited clinical success due to poor bioavailability. Considering the lipophilic nature of VCO, curcumin added to VCO is expected to have synergistic/additive actions. In this study, the chemopreventive potential of curcumin enriched VCO (VCr) (4 and 8 mL/Kg orally) was analyzed in 7,12-dimethyl benz[a]anthracene (DMBA;470 nmoles/200 µL/week for two weeks topical)/croton oil (3% v/v in 200 µL acetone twice a week for 6 weeks topical) induced skin papilloma. In DMBA control animals, an average incidence of 13 papilloma/mice (latency period of 11.6 ± 1.5 weeks) was recorded. Pretreatment with VCrH (8 mL/kg) had a 60% inhibition of tumor index, and an increased latency period (12.5 ± 0.9 weeks). Additionally, DMBA/croton oil-induced reduction in glutathione levels and concomitant increase in thiobarbituric acid reactive substance (TBARS) in the skin microenvironment were restored by VCr. The study thus suggests that the VCr promotes antioxidant status in vivo and imparts an improved anticarcinogenic potential. However, further studies are necessary to ascertain the improvement in bioavailability of curcumin .

Non-polar lipid carbonyls of thermally oxidized coconut oil induce hepatotoxicity mediated by redox imbalance.

Thermal oxidation products of edible oils including aldehydes, peroxides and polymerized triglycerides formed during the cooking process are increasingly debated as contributory to chronic degenerative diseases. Depending on the oil used for cooking, the source of fatty acids and its oxidation products may vary and would have a differential influence on the physiological process. Coconut oil (CO) is a medium chain triglyceride-rich edible oil used in South India and other Asia Pacific countries for cooking purposes. The present study evaluated the biological effects of thermally oxidized coconut oil (TCO) as well as its non- polar hexane (TCOH) and polar methanol (TCO-M) sub-fractions in male Wistar rats. Results showed an increase in the thiobarbituric acid reactive substances (TBARs) and conjugated diene levels in TCO, which was extracted to TCOH fraction. The animals consumed TCO and its hexane and methanol fractions had a considerable increase in weight gain. However, serum and hepatic triglycerides were increased only in animals with TCO and TCOH administration. In these animals, the hepatic redox balance was disturbed, with a reduction in GSH and a concomitant increase in thiobarbituric acid reactive substances (TBARs). Increased incidence of microvesicles in hepatic histological observations also supported this assumption. Together, the study shows that TCO consumption is unhealthy, where the nonpolar compounds generated during thermal oxidation may be involved in the toxic insults.

Polyphenols of virgin coconut oil prevent pro-oxidant mediated cell death.

Virgin coconut oil (VCO), extracted from the fresh coconut kernel, is a food supplement enriched with medium chain saturated fatty acids and polyphenolic antioxidants. It is reported to have several health benefits including lipid lowering, antioxidant and anti-inflammatory activities. The pharmacological benefits of VCO have been attributed to its polyphenol content (VCOP), the mechanistic basis of which is less explored. Liquid chromatography/mass spectroscopy (LC/MS) analysis of VCOP documented the presence of gallic acid, ferulic acid (FA), quercetin, methyl catechin, dihydrokaempferol and myricetin glycoside. Pre-treatment of VCOP at different concentrations (25-100 µg/mL) significantly reduced the H2O2 and 2,2'-azobis (2-amidinopropane) dihydrochloride (AAPH) induced cell death in HCT-15 cells. Giving further insight to its mechanistic basis, oxidative stress induced alterations in glutathione (GSH) levels and activities of GR (Glutathione-Reductase), GPx (Glutathione-Peroxidase), GST (Glutathione-S-Transferase) and catalase (CAT) were restored to near-normal by VCOP, concomitantly reducing lipid peroxidation. The efficacy of VCOP was similar to that of Trolox and FA added in culture. The study thus suggests that VCOP protects cells from pro-oxidant insults by modulating cellular antioxidant status.