44 research outputs found
Change and Aging Senescence as an adaptation
Understanding why we age is a long-lived open problem in evolutionary
biology. Aging is prejudicial to the individual and evolutionary forces should
prevent it, but many species show signs of senescence as individuals age. Here,
I will propose a model for aging based on assumptions that are compatible with
evolutionary theory: i) competition is between individuals; ii) there is some
degree of locality, so quite often competition will between parents and their
progeny; iii) optimal conditions are not stationary, mutation helps each
species to keep competitive. When conditions change, a senescent species can
drive immortal competitors to extinction. This counter-intuitive result arises
from the pruning caused by the death of elder individuals. When there is change
and mutation, each generation is slightly better adapted to the new conditions,
but some older individuals survive by random chance. Senescence can eliminate
those from the genetic pool. Even though individual selection forces always win
over group selection ones, it is not exactly the individual that is selected,
but its lineage. While senescence damages the individuals and has an
evolutionary cost, it has a benefit of its own. It allows each lineage to adapt
faster to changing conditions. We age because the world changes.Comment: 19 pages, 4 figure
Evidence of a systemic phenomenon for oxidative stress in cholestatic liver disease
BACKGROUND—There is considerable evidence indicating that the severity of hepatic damage in individuals with cholestatic liver disease is causally associated with the extent of intrahepatic oxidative stress. Increased levels or accelerated generation of reactive oxygen species and toxic degradative products of lipid peroxidation have been reported in the plasma of individuals with chronic liver disease and animal models of liver disease. Hence, by virtue of their increased presence in the circulation, it is not unreasonable to suppose that they may account for extrahepatic tissue damage in chronic liver disease.
MATERIALS AND METHODS—This hypothesis was tested by determining plasma levels of the ubiquitous antioxidant glutathione (GSH) and lipid peroxides (LP), together with assessment of the extent of lipid peroxidation in the kidney, brain, and heart, in 24 day chronically bile duct ligated (CBDL) rats. The extent of lipid peroxidation in tissues was based on measurement of conjugated dienes, lipid peroxides, and malondialdehyde (MDA) content. Data were compared with identical data collected from unoperated control, pair fed, 24 day bile duct manipulated (sham operated), and pair fed sham operated rats.
RESULTS—In CBDL rats, total and reduced plasma GSH levels were almost half those determined in all control rats. Plasma, kidney, and heart LP levels were significantly increased in CBDL rats compared with controls. MDA levels were significantly higher in the kidney, brain, and heart homogenates prepared from CBDL rats compared with MDA content measured in tissue homogenates prepared from the four groups of control rats.
CONCLUSIONS—Our data show that experimental cholestatic liver disease is associated with increased lipid peroxidation in the kidney, brain, and heart. Hence we have concluded that the oxidative stress in cholestatic liver disease is a systemic phenomenon probably encompassing all tissues and organs, even those separated by the blood-brain barrier.
Keywords: cirrhosis; oxidative stress; lipid peroxidation; lipid peroxides; conjugated dienes; malondialdehyde; glutathion