The article by E. D. Wills investigates the mechanisms of lipid peroxide formation in animal tissues, specifically focusing on rat liver, spleen, heart, and kidney. Key findings include: 1. **Homogenates Catalyze Peroxide Formation**: Homogenates of these tissues form lipid peroxides when incubated in vitro and catalyze peroxide formation in emulsions of linoleic or linolenic acid. 2. **Catalytic Activity Distribution**: Catalytic activity is distributed throughout the nuclear, mitochondrial, and microsomal fractions of liver homogenates, with the 100,000g supernatant showing weak activity. 3. **pH and Concentration Effects**: Dilute homogenates catalyze peroxidation over a pH range of 5.0-8.0, while concentrated homogenates (5%, w/v) inhibit peroxidation and destroy peroxide if the solution is more alkaline than pH 7.0. 4. **Ascorbic Acid Influence**: Ascorbic acid increases the rate of peroxidation of unsaturated fatty acids catalyzed by whole homogenates and mitochondrial fractions but inhibits it in the supernatant fraction. 5. **Iron and Ferritin Role**: Inorganic iron and ferritin are active catalysts in the presence of ascorbic acid. Ferritin, when treated with hydrogen peroxide, releases iron, which becomes an effective catalyst. 6. **Chelating Agents**: EDTA strongly inhibits iron-catalyzed peroxidation but has little effect on haemoprotein-catalyzed oxidation. O-phenanthroline stimulates peroxidation by iron but inhibits it by haemoproteins. 7. **Thiol Compounds**: Cysteine and glutathione (GSH) inhibit peroxidation by haemoproteins but can enhance it by non-haem iron at higher concentrations. The study highlights the complex roles of non-haem iron and haemoproteins in lipid peroxide formation, emphasizing the importance of pH and tissue-specific factors. The findings suggest that lipid peroxide formation in vivo can have significant cellular consequences, including membrane damage and enzyme inactivation.The article by E. D. Wills investigates the mechanisms of lipid peroxide formation in animal tissues, specifically focusing on rat liver, spleen, heart, and kidney. Key findings include: 1. **Homogenates Catalyze Peroxide Formation**: Homogenates of these tissues form lipid peroxides when incubated in vitro and catalyze peroxide formation in emulsions of linoleic or linolenic acid. 2. **Catalytic Activity Distribution**: Catalytic activity is distributed throughout the nuclear, mitochondrial, and microsomal fractions of liver homogenates, with the 100,000g supernatant showing weak activity. 3. **pH and Concentration Effects**: Dilute homogenates catalyze peroxidation over a pH range of 5.0-8.0, while concentrated homogenates (5%, w/v) inhibit peroxidation and destroy peroxide if the solution is more alkaline than pH 7.0. 4. **Ascorbic Acid Influence**: Ascorbic acid increases the rate of peroxidation of unsaturated fatty acids catalyzed by whole homogenates and mitochondrial fractions but inhibits it in the supernatant fraction. 5. **Iron and Ferritin Role**: Inorganic iron and ferritin are active catalysts in the presence of ascorbic acid. Ferritin, when treated with hydrogen peroxide, releases iron, which becomes an effective catalyst. 6. **Chelating Agents**: EDTA strongly inhibits iron-catalyzed peroxidation but has little effect on haemoprotein-catalyzed oxidation. O-phenanthroline stimulates peroxidation by iron but inhibits it by haemoproteins. 7. **Thiol Compounds**: Cysteine and glutathione (GSH) inhibit peroxidation by haemoproteins but can enhance it by non-haem iron at higher concentrations. The study highlights the complex roles of non-haem iron and haemoproteins in lipid peroxide formation, emphasizing the importance of pH and tissue-specific factors. The findings suggest that lipid peroxide formation in vivo can have significant cellular consequences, including membrane damage and enzyme inactivation.