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Oxidative removal of the N-ethoxymethyl group of Chlorfenapyr by mixed function oxidases forms uncouples oxidative phosphorylation at the mitochondria, resulting in disruption of production of ATP, cellular death, and ultimately organism mortality [3].
Necrosis is a process of cellular death and tissue damage initiated typically by the molecules of inflammation.
In the development of the aerenchyma of the expansigeny type, found in the families Polygonaceae and Pontederiaceae, the expansion of intercellular spaces originates gaps without causing collapse or cellular death.
A receptor carried in abundance by neurons, P2X7, lets the ATP latch onto motor neurons, which leads to cellular death and worsens the injury.
After this "point of no return" most probably due the combined damage by ROS to cellular membranes, transport systems and mitochondria, cellular death is inevitably initiated and no longer under control by antioxidants.
Among the adverse effects observed were mitochondrial structural decomposition, mitochondrial swelling due to increased membrane porosity and rupturing, increased production of free radicals, and induction of cellular death.
This is crucial to understanding photosensitivity and lupus because TNF-alpha has been shown to stimulate apoptosis, the process of cellular death.
Cellular death seems a fundamental axis in the embryo organization since its early stages: in a mouse blastocyst, relevant cell death is observed in vivo, suggesting that it plays an important role in normal development.
The zone of thermal necrosis was defined as that area of meniscus with cellular death and lack of extracellular matrix.
72-78) The role of ROS in promoting cellular death in the inner ear and the protective effects of antioxidants and ROS scavengers in attenuating ischemia/reperfusion-induced and noise-induced cochlear damage have been substantiated in many animal studies.
Free radicals create a cellular death spiral by mutating mitochondrial DNA, which in turn degrades their energy production and increases the production of free radicals, refueling the cycle.
Scientists seek answers to these questions out of a desire to tinker with the mechanisms of cellular death, not just in the blood but throughout the body.
Infusion of L-asparaginase destroys the external source of asparagine, which starves leukaemia cells of this amino acid and leads to cellular death.
Short telomeres are associated with premature cellular death.