Ferritin and neuromelanin may contribute to neuroprotection [ 36], since free cytosolic iron can trigger oxidative stress and promote α-SN deposition in Lewy bodies [ 28, 37].
Latest evidence suggests, however, that bacterial LPS deriving from the gut microbiota may trigger inflammation and oxidative stress in response to diets (4, 6, 21– 21).
Nanoparticles may trigger cytotoxic effects, and oxidative stress induction has been proposed as a common paradigm for the cellular toxicity of nanoparticles.
In the presence of excess iron, exogenous oxidative toxins, such as lead, may trigger the Fenton reaction, enhancing oxidative stress.
Oxidative stress may trigger steatohepatitis by three main mechanisms: lipid peroxidation, cytokine induction, and induction of Fas ligand.
There is a consensus that ANG II may trigger vascular inflammation by inducing oxidative stress and upregulation of pro-inflammatory transcription factors such as nuclear factor kappa B (NF-κB).
While the long-term effects of subtle hypoxia on brain tissue are not fully understood, it is becoming increasingly clear that oxidative stress may trigger neuropathological processes both local and distal to the site of mild brain contusion, effects which may only manifest themselves months to years later [ 31].
In conclusion, chronic SM exposure may have the potential to generate oxidative stress which may trigger the release of cytochrome c as well as caspase-3 activation in neurons leading to cell death by apoptosis in a dose dependent manner which may in the end be responsible for the disruption of cognitive functions in mice.
We demonstrated that RPE dysfunction might lead to dysregulation of macrophage clearance function and angiogenic homeostasis as a result of oxidative damage which may trigger progression towards CNV in smoker patients with dry AMD.
