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Moreover, mitochondrial dysfunction and related oxidative stress can activate the innate branch of the immune system, leading to the release of pro-inflammatory cytokines influencing various depression-related pathophysiological mechanisms: monoaminergic neurotransmission disruption, tryptophan degradation toward neurotoxic catabolites, glutamate-related excitotoxicity, decreased neurotrophic factors and alterations in the hypothalamic-pituitary-adrenal axis [3, 33, 59]
Combining the two might theoretically exacerbate digestive symptoms in susceptible individuals, though this has not been systematically studied
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The occlusion cases ratio was up to ~76% at 1.5 mM of tBuOOH (Supplementary Fig
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