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Fenton reactions, characterized as redox processes, are instigated by minerals renowned for their oxidative attributes - specifically iron and copper. Due to their elevated oxidative potential, such minerals readily seize electrons from surrounding molecules.

Cu²⁺ + O₂ → Cu⁺ + O₂⁻ Fe3⁺ + O₂ → Fe2⁺ + O₂⁻ Fenton reactions

Henry Fenton, a British chemist in the 1890s, elucidated these reactions where iron and copper act as catalysts in spawning highly reactive hydroxyl radicals from hydrogen peroxide. The radicals produced are particularly reactive, triggering extensive cellular lipids, proteins, and DNA oxidation.

When hydroxyl radicals assail polyunsaturated fatty acids in membrane lipids, membrane integrity becomes jeopardized. This may lead to compromised cellular functions or even cell death. Similarly, radicals can oxidize amino acids, transforming protein structures and hindering cellular activities. In the realm of DNA, radicals predominantly target the deoxyribose backbone.

Enterocytes and Hepatocytes, the primary mineral absorption and storage channels, are the most susceptible to Fenton reactions. Hepatocytes' heightened metabolic activity necessitates significant mitochondrial functionality, rendering them susceptible to damage from hydroxyl radicals. These disruptions can activate inflammatory responses and mobilize immune cells.

Muscle metabolism too isn't spared from the clutches of radicals. Elevated lipid oxidation modifies the fatty acid profile, inducing off-flavours due to secondary oxidation products. Oxidative reactions can turn muscle myoglobin into metmyoglobin, presenting a less appealing brownish colour. Additionally, lipid membrane alterations in muscle cells can influence meat's water-holding capacity, thus affecting its texture and juiciness.

Although both copper and iron facilitate hydroxyl radical generation, copper is often deemed a more powerful oxidant, especially given its prowess to infiltrate membranes and localize in sensitive areas like the nucleus. Iron, however, is efficiently sequestered by cellular mechanisms like ferritin, minimizing its participation in Fenton reactions.

Yet, copper's oxidative potency is form-dependent. While divalent copper (Cu2+) boasts robust oxidant properties, monovalent copper (Cu+) operates as a reduction, devoid of oxidative capabilities. Interestingly, the predominant form of copper in animal nutrition is divalent, commonly found in compounds like Copper Sulfate and Copper Chloride. During absorption, while part of the copper maintains its divalent form, some transform into monovalent copper, facilitating absorption through the CTR1 transporter.

However, excess of dietary copper can amplify intestinal absorption, inundating hepatic and systemic circulations with copper. Such surges can overwhelm cellular mechanisms, leading to elevated free copper levels inside cells.

In intensive Swine and Poultry production, animals consistently grapple with pro-oxidative elements, hampering their growth and yield. Excess of oxidative minerals is one of the major favouring mechanisms leading to oxidative challenges for animals. It is important that nutritionists take the oxidative potency of the diet into consideration when they formulate. They should look at reducing exposure to excessive levels of minerals for too long periods, especially copper or they can select a monovalent form to reduce the oxidative risks on animals.

Through vigilant management of a diet's oxidative status, one can potentially amplify animal growth performance, simultaneously enhancing meat's flavour, texture, and colour.


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