Biological method for the assessment of leaching rates of antifouling compositions

Rivett, P.

doi:10.1002/jctb.5010151006

Cited by 10 publications

(1 citation statement)

References 2 publications

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“…Secondly, the half-life of oxidized macromolecules is often shorter than that of the parent molecules. The former are generally selectively degraded, repaired and/or replaced by nascent biosynthesis 100, 109, 110 . Thus the steady-state levels of modified macromolecules are a snapshot of the dynamic balance between the processes of degradation, repair and biosynthesis rather than a measure of the cumulative damage.…”

Section: Testing Of the Structural Damage-based Oxidative Stress Hypomentioning

confidence: 99%

The redox stress hypothesis of aging

Sohal

Orr

2012

Free Radical Biology and Medicine

422

343

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The main objective of this review is to examine the role of the endogenous reactive oxygen/nitrogen species (ROS) in the aging process. Until relatively recently, ROS were considered to be potentially toxic by-products of aerobic metabolism, which, if not eliminated, may inflict structural damage on various macromolecules. Accrual of such damage over time was postulated to be responsible for the physiological deterioration in the post-reproductive phase of life and eventually the death of the organism. This “structural damage-based oxidative stress” hypothesis has received support from the age-associated increases in the rates of ROS production and the steady-state amounts of oxidized macromolecules; however, there are increasing indications that structural damage alone is insufficient to satisfactorily explain the age-associated functional losses. The level of oxidative damage, accrued during aging, often does not match the magnitude of functional losses. Although experimental augmentations of antioxidant defenses tend to enhance resistance to induced oxidative stress, such manipulations are generally ineffective in the extension of life span of long-lived strains of animals. More recently, in a major conceptual shift, ROS have been found to be physiologically vital for signal transduction, gene regulation and redox regulation, among others, implying that their complete elimination would be harmful. An alternative notion, advocated here, termed “redox stress hypothesis”, proposes that aging-associated functional losses are primarily caused by a progressive pro-oxidizing shift in the redox state of the cells, which leads to the over-oxidation of redox-sensitive protein thiols and the consequent disruption of the redox-regulated signaling mechanisms.

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Section: Testing Of the Structural Damage-based Oxidative Stress Hypomentioning

confidence: 99%