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Mechanisms of lipid peroxide formation in animal tissues.

Wills Ed
- 01 Jun 1966 - 
- Vol. 99, Iss: 3, pp 667-676
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TLDR
Catalysis of peroxidation of unsaturated fatty acids by the mitochondrial and microsomal fractions of liver is inhibited by ascorbic acid at pH7.4 but the activity of the supernatant fraction is enhanced.
Abstract
1. Homogenates of rat liver, spleen, heart and kidney form lipid peroxides when incubated in vitro and actively catalyse peroxide formation in emulsions of linoleic acid or linolenic acid. 2. In liver, catalytic activity is distributed throughout the nuclear, mitochondrial and microsomal fractions and is present in the 100000g supernatant. Activity is weak in the nuclear fraction. 3. Dilute (0.5%, w/v) homogenates catalyse peroxidation over the range pH5.0-8.0 but concentrated (5%, w/v) homogenates inhibit peroxidation and destroy peroxide if the solution is more alkaline than pH7.0. 4. Ascorbic acid increases the rate of peroxidation of unsaturated fatty acids catalysed by whole homogenates of liver, heart, kidney and spleen at pH6.0 but not at pH7.4. 5. Catalysis of peroxidation of unsaturated fatty acids by the mitochondrial and microsomal fractions of liver is inhibited by ascorbic acid at pH7.4 but the activity of the supernatant fraction is enhanced. 6. Inorganic iron or ferritin are active catalysts in the presence of ascorbic acid. 7. Lipid peroxide formation in linoleic acid or linolenic acid emulsions catalysed by tissue homogenates is partially inhibited by EDTA but stimulated by o-phenanthroline. 8. Cysteine or glutathione (1mm) inhibits peroxide formation catalysed by whole homogenates, mitochondria or haemoprotein. Inhibition increases with increase of pH.

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Hempseed (Cannabis sativa) lipid fractions alleviate high-fat diet-induced fatty liver disease through regulation of inflammation and oxidative stress

TL;DR: HEMP administration to hypercholesterolemic rats resolved the morphological, histopathological, and biochemical indicators of fatty liver diseases and the mechanistic evidence revealed that these hepatoprotective effects of HEMP are mediated through inhibition of oxidative stress and inflammatory mediators such as Cox-2, hPGDS, mPGES, IL-4, TNF-α and sEH.
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NADPH-induced chemiluminescence and lipid peroxidation in kidney microsomes.

TL;DR: The results which demonstrate the production of excited states and LP by renal microsomes suggest that their role in renal disease deserves further study and suggest that other free radical mechanisms are likely to be important in the CL and LP responses.
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Lipid peroxidation in vitro by isolated fat cells of rats. Correlation with total lipolysis, glucose utilization, and dietary tocopherol.

TL;DR: It is concluded that the thiobarbituric acid test, applied to fat cells, is not an indicator of total lipolysis, nor of vitamin E deficiency, and fat cell glucose utilization andlipolysis are not altered by either vitamin E deficiencies or increased lipid peroxidation.
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Antioxidant activity of catechins isolate of uncaria gambier roxb in male rats

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Antihyperglycemic and antioxidant activity of Clitorea ternatea Linn. on streptozotocin-induced diabetic rats.

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References
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Journal ArticleDOI

Mechanisms of lipid peroxide formation in tissues. role of metals and haematin proteins in the catalysis of the oxidation unsaturated fatty acids.

TL;DR: Oxidation of unsaturated fatty acids such as linoleic acid and linolenic acid is catalysed by metals at 37° in the pH range 4.5–7.5 with the formation of peroxides and it is considered that, in vivo, lipid peroxide formation is likely to be a result of oxidation of uns saturated lipids.
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