If we eat anti-oxidants, we can prevent our mitochondria from being damaged by
excessive reactive oxygen species.
Fat cells produce
excessive reactive oxygen species, which can damage cells in a process called oxidative stress.
Not exact matches
Also, in both cell culture and a mouse model of the condition, blocking the
excessive splintering reduced production of
reactive oxygen species, a potentially harmful byproduct of metabolism, as well as cell death.
Although many years ago we found that
reactive oxygen species (ROS) are required for full expression of hippocampal LTP and memory, it is clear that the aged and diseased brain handle ROS much differently as many studies have pointed to a role for
excessive ROS and oxidative stress in age - related cognitive decline and impaired memory associated with Alzheimer's disease (AD).
It prevents hyperglycemic toxicity to neurons, pancreatic cells, the arterial walls and the generation of
excessive levels of
reactive oxygen species.
Generation of
reactive oxygen species, or free radicals such as superoxide and hydrogen peroxide, is a normal byproduct of metabolism, but can damage cellular machinery when
excessive and impair the production of cellular energy, which becomes a vicious cycle as energy - intensive repair processes become untenable (25, 26).