Lipid peroxide formation in animal tissues is catalyzed by various components, including haemoproteins and inorganic iron. Tissue homogenates from rat liver, spleen, heart, and kidney catalyze peroxide formation in emulsions of unsaturated fatty acids like linoleic and linolenic acid. Catalytic activity is distributed in nuclear, mitochondrial, and microsomal fractions, with the 100000g supernatant also showing activity. The rate of peroxidation is influenced by pH, with higher rates at lower pH values. Ascorbic acid enhances peroxidation at pH 6.0 but not at pH 7.4, while it inhibits peroxidation in mitochondrial and microsomal fractions at pH 7.4. Inorganic iron or ferritin are active catalysts in the presence of ascorbic acid. EDTA inhibits peroxidation, while o-phenanthroline stimulates it. Cysteine or glutathione inhibits peroxide formation, with inhibition increasing with pH. Lipid peroxide formation is toxic and may result from oxidative damage to thiol groups in proteins and enzymes. It can also cause membrane damage, as seen in erythrocytes and lysosomes. In vivo, lipid peroxide formation is likely to cause severe cellular damage, though accurate analysis is challenging. Studies in vitro show that most animal tissues form thiobarbituric acid reactants when incubated under aerobic conditions. These are believed to be formed by the oxidation of unsaturated fatty acids in tissue lipids, possibly via hydroperoxides. Two systems are involved in peroxide formation: haemoproteins like haemoglobin and cytochrome c, and non-haem iron. Ascorbic acid stimulates peroxidation in some tissues but inhibits it in others. The thiobarbituric acid method measures degradation products of peroxidized fats, which may not directly reflect lipid peroxide levels. Experiments using emulsions of unsaturated fatty acids allow for the study of oxidation and peroxide formation, including oxygen uptake and other methods. Tissue homogenates from liver, kidney, spleen, and heart catalyze peroxidation of linoleic and linolenic acid. The rate of peroxidation is influenced by homogenate concentration, pH, and the presence of ascorbic acid or other compounds. Haemoproteins are active catalysts in dilute solutions but inhibit peroxidation in concentrated solutions. Non-haem iron, when released from ferritin by ascorbic acid, becomes a catalyst. Iron content varies among tissues, with spleen having the highest haem iron content. Catalytic activity in liver fractions is present in mitochondria, microsomes, and the supernatant, with ascorbic acid affecting these activities. o-PhenanthroLipid peroxide formation in animal tissues is catalyzed by various components, including haemoproteins and inorganic iron. Tissue homogenates from rat liver, spleen, heart, and kidney catalyze peroxide formation in emulsions of unsaturated fatty acids like linoleic and linolenic acid. Catalytic activity is distributed in nuclear, mitochondrial, and microsomal fractions, with the 100000g supernatant also showing activity. The rate of peroxidation is influenced by pH, with higher rates at lower pH values. Ascorbic acid enhances peroxidation at pH 6.0 but not at pH 7.4, while it inhibits peroxidation in mitochondrial and microsomal fractions at pH 7.4. Inorganic iron or ferritin are active catalysts in the presence of ascorbic acid. EDTA inhibits peroxidation, while o-phenanthroline stimulates it. Cysteine or glutathione inhibits peroxide formation, with inhibition increasing with pH. Lipid peroxide formation is toxic and may result from oxidative damage to thiol groups in proteins and enzymes. It can also cause membrane damage, as seen in erythrocytes and lysosomes. In vivo, lipid peroxide formation is likely to cause severe cellular damage, though accurate analysis is challenging. Studies in vitro show that most animal tissues form thiobarbituric acid reactants when incubated under aerobic conditions. These are believed to be formed by the oxidation of unsaturated fatty acids in tissue lipids, possibly via hydroperoxides. Two systems are involved in peroxide formation: haemoproteins like haemoglobin and cytochrome c, and non-haem iron. Ascorbic acid stimulates peroxidation in some tissues but inhibits it in others. The thiobarbituric acid method measures degradation products of peroxidized fats, which may not directly reflect lipid peroxide levels. Experiments using emulsions of unsaturated fatty acids allow for the study of oxidation and peroxide formation, including oxygen uptake and other methods. Tissue homogenates from liver, kidney, spleen, and heart catalyze peroxidation of linoleic and linolenic acid. The rate of peroxidation is influenced by homogenate concentration, pH, and the presence of ascorbic acid or other compounds. Haemoproteins are active catalysts in dilute solutions but inhibit peroxidation in concentrated solutions. Non-haem iron, when released from ferritin by ascorbic acid, becomes a catalyst. Iron content varies among tissues, with spleen having the highest haem iron content. Catalytic activity in liver fractions is present in mitochondria, microsomes, and the supernatant, with ascorbic acid affecting these activities. o-Phenanthro