Free radicals in immunological killing: The case of tumour necrotising factor (TNF)
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Radiation takes its Toll
2015, Cancer LettersCitation Excerpt :The infiltration of immune cells that TLR signaling generates, initially innate players such as polymorphs then monocytes, possibly followed by lymphocytes, drives a pro-inflammatory, pro-oxidant environment – i.e. a bona fide inflammatory response and eventually turns it into one that will allow resolution of inflammation, tissue repair, regeneration and healing [41,42] and/or in the case of lymphocyte involvement, immune reactivity. It is in the nature of an inflammatory response to cause additional tissue damage – at least initially – through excessive Reactive Oxygen or Nitrogen Species (ROS/RNS) production, proteolytic enzyme activity and self-perpetuating cytokine loops [42–44]. This is the point of contact with radiation that generates ROS/RNS, a response that is perpetuated by pro-inflammatory cytokines further driving ROS/RNS production including superoxide anion, hydroxyl radicals, hydrogen peroxide, nitric oxide, peroxinitrite and others [45,46].
Could oxidative stress initiate programmed cell death in HIV infection? A role for plant derived metabolites having synergistic antioxidant activity
1994, Chemico-Biological InteractionsCell killing and induction of manganous superoxide dismutase by tumor necrosis factor-(α is mediated by lipoxygenase metabolites of arachidonic acid
1992, Biochemical and Biophysical Research Communications