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To avoid metHb accumulation, reducing pathways mediated by cytochrome b5 or flavin coupled with NADH- or NADPH-dependent metHb reductases (MHbR), respectively, keep the level of metHb in erythrocytes at less than 1% of the total Hb under normal conditions (48)

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after its in vivo conversion in arachidonic acid antagonist, and in presence of GSH as biological catalyst, CLA inhibits the formation of Prostaglandin E2, anti-inflammatory mediator

Neuroinflammation or fever is presumed to also trigger ISR, as autoantibodies may target neural or immune systems and cause inflammation elsewhere (418)