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For example, the ingestion of trimethylamine-containing (TMA-containing) dietary nutrients enriched in animal products such as choline, phosphatidylcholine, and l-carnitine can serve as precursor for the ultimate generation of an atherogenic metabolite, trimethylamine N -oxide (TMAO), via a metaorganismal pathway involving initial gut microbial formation of TMA, followed by host hepatic conversion of TMA into TMAO (48)

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This imbalance is also associated with excessive superoxide production and mitochondrial DNA damage [197]

Abnormal hepatic mitochondrial respiration and cytochrome C oxidase activity in rats with long-term copper overload

Circulating Fe 3+ enters cells with the assistance of transferrin and subsequently converts to Fe 2+ ( 2+ can catalyze the generation of metabolically toxic reactive oxygen species and phospholipid peroxide through the Fenton reaction, leading to cell damage or death (Figure 4)