Liver oxidized oils

Moderately thermally oxidized soybean oil (130°C, air flow-through) of peroxide value (PV) = 75 mEq 02/kg diet (compared with the control of 9.5 Eq 02/kg diet) was fed to rats for 40 days (Eder and Kirchgessner, 1999). The study showed no adverse effects on liver, heart, kidney, or adipose tissue FA composition, and even a reduction in the osmotic fragility of erythrocytes and hepatic lipogenesis. However, the moderately oxidized oil slightly reduced the vitamin E status in the tissues. A slightly increased susceptibility of LDL to lipid peroxidation, and an increased concentration of thiobarbituric acid reactive substances (TEARS) in LDL, were also observed. 

Kimura, Y, H. Ohminami, and H. Okuda. 1983. Effects of stilbene components of roots of Polygonum spp. on liver injury in per-oxidized oil-fed rats. Planta Med. 49(l) 51-54. 

Koch, A., B. Kbnig, J. Spielmann, A. Leitner, G.l. Stangl, and K. Eder. 2007a. Thermally oxidized oil increases the expression of insulin-induced genes and inhibits activation of sterol regulatory element-binding protein-2 in rat liver. Journal of Nutrition 137 2018-23. 

Varady, J., D.K. Gessner, E. Most, K. Eder, and R. Ringseis. 2012a. Dietary moderately oxidized oil activates the Nif2 signaling pathway in the liver of pigs. Ilnids Health Disease 11 31. 

Oils that have undergone lipid peroxidation may have adverse physiological effects if consumed. Eor example, Eder (1999) found that oxidized oils in a diet could diminish the ability of rat heart and liver tissues to desaturate fatty acids. Work by Sheehy et al. in 1994 showed that the consumption of thermally oxidized sunflower oil by chicks reduces the tissue content of a-tocopherol and increases the susceptibility of tissues to lipid peroxidation. The addition of vitamin E to refined olive oil increases the stability of the oil under pro-oxidant conditions and decreases the oxidative damage caused by adriamycin in rats (Quiles et al., 1999). 

Mineral Oil Hydraulic Fluids. No studies regarding hepatic effects in humans following inhalation, oral, or dermal exposure to mineral oil hydraulic fluids were located. In an animal study, histopathological examination of the livers from rats exposed by inhalation to <1.0 mg/m3 of the water-in-oil emulsion hydraulic fluid Houghto-Safe 5047F for 90 days, 23 hours/day, showed no treatment-related lesions (Kinkead et al. 1991). Animal data for oral exposure are limited to one study where rats were exposed to MIL-H-5606 at 1,000 mg/kg/day for 26 days (Mattie et al. 1993). Increases in liver weight and peroxisomal beta-oxidation activity were observed. 

On the other hand, in rats, a single dose of 6,156 mg/kg hexachloroethane in mineral oil had no effects on a different set of biochemical indicators of liver function (microsomal protein, oxidative demethylase, NADP-NT reductase, glucose-6-phosphatase, or lipid conjugated diene concentration) when measured 2 hours after compound administration (Reynolds 1972). Each of these parameters is an indicator of microsomal function. The authors postulated that the observed lack of effects could have been the result of slow uptake of hexachloroethane by the liver in a 2-hour period. Gastrointestinal absorption of hexachloroethane in mineral oil is probably minimal because, unlike olive oil, mineral oil cannot be digested. Dissolved lipophilic materials could be excreted in the feces soon after administration because mineral oil can act as a laxative. Thus, the author s hypothesis that minimal hexachloroethane would reach the liver in 2 hours is reasonable. 

The key experiments leading to the identification of vitamin D were those of Mellanby (1918-1919) using puppies. When they were fed on bread, skimmed milk, linseed oil, yeast (to give B vitamins), and orange juice (vitamin C) the puppies developed rickets. When cod-liver oil and/or butter were added, rickets was prevented. The distinction between the effects of vitamin A and the anti-rachitic factor was aided by the sensitivity of vitamin A to oxidation. Aerated (oxidized) cod-liver oil no longer cured xerophthalmia but its anti-rachitic properties were unaffected (McCollum, 1922). 

Medium-chain fatty acids are also present in bovine milk and some plant oils (e.g. coconut). After digestion of the triacylglycerol, they are taken up by the enterocytes in the small intestine but are not esterified. Instead they pass directly into the hepatic portal blood, from where they are taken up by the liver for complete oxidation or conversion to ketone bodies. 

CN184 Plot. C., ]. F. Hocquette, ]. H. Veerkamp, D. Durand, and D. Bauchart. Effects of dietary coconut oil on fatty acid oxidation capacity of the liver, the heart and skeletal muscles in... 

Antioxidant activity was also tested in a liver microsome system. In this study, mice were treated by oral intubation (2 times/wk) with 0.2 ml olive oil alone or containing CLA (0.1 ml), linoleic acid (0.1 ml), or dl-a-tocopherol (lOmg). Four weeks after the first treatment, liver microsomes were prepared and subsequently subjected to oxidative stress using a non-enzymatic iron-dependent lipid peroxidation system. Microsomal lipid peroxidation was measured as thiobarbituric acid-reactive substance (TBARS) production using malondialdehyde as the standard. It was found that pretreatment of mice with CLA or dl-a-tocopherol significantly decreased TBARS formation in mouse liver microsomes (p < 0.05) (Sword, J. T. and M. W. Pariza, University of Wisconsin, unpublished data). 

The all-tra 5 -squalene (C30H50), discovered in shark liver oil in the 1920s, is a triterpene, but one in which the isoprene rule at violated in one point. Rather than a head-to-tail arrangement of six units of isoprene, there appear to be farnesyl units that have been connected tail to tail. Almost aU steroids are biosynthesized from cholesterol. Cholesterol is biosynthesized from squalene, which is first converted to lanosterol. The conversion of squalene to the steroid skeleton is an oxirane, squalene-2,3-oxide, which is transformed by enzymes into lanosterol, a steroid alcohol naturally found in wool fat. The whole process is highly stereoselective. 

Antagonists of the tocopherols indude a-tocopherol qtiinone. oxidants, cod liver oil, and thyroxine. Synergists include ascorbic acid, estradiol,... 

The safety of drugs containing EPA and DHA has been reviewed the reported adverse effects were similar to those in control groups (3). Even 3-7 g/day for several months did not change liver enzyme activities, and there were no bleeding problems. Consumption of fish oils reduces the resistance of LDL to oxidative modification, and this is partly opposed by the addition of vitamin E (4). Belching or eructation with a fishy taste or smell, vomiting, flatulence, diarrhea, and constipation are relatively common. 

Biochemical stress can be minimized by using frequent feedings to minimize dependence on fatty acid oxidation, particularly for the liver. Meals should have a high-carbohydrate, low-fat content. Medium-chain triglycerides (synthetic or derived from coconut or palm kernel oils) can be used as these lipids can be oxidized independent of carnitine. These steps are particularly important when any external metabolic stress, such as a viral illness, is present. 

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