Aspects of Free Radical Reactions in Biological Systems: Aging

Leibovitz, Brian; Siegel, Benjamin V.

doi:10.1093/geronj/35.1.45

Cited by 303 publications

(88 citation statements)

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“…The mechanism of aging at the biochemical level can be explained by the production of free radicals, which are induced by oxidative stress, resulting in the cellular membrane damage. Free radicals attack proteins, nucleic acids, carbohydrates and lipids of the cells (Gunther et al, 1991;Leibovitz et al, 1980;Sohal et al, 2002). It is widely accepted that free radicals induce LPO and play an important role in agerelated pathological phenomena including the clustering of degenerative diseases (Gunther et al, 1991;Harman, 1981;Tokumaru et al, 1996).…”

Section: Resultsmentioning

confidence: 99%

Effect of Royal Jelly Diet on the Testicular Function of Hamsters

Kohguchi¹,

Inoue²,

Ushio³

et al. 2004

FSTR

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To investigate the long-term effect of feeding royal jelly (RJ) on the testicular function, 32-week old male golden hamsters were fed diet containing RJ at doses of O ug/g diet (control), 50 ug/g diet or 500 ug/g diet for 12 weeks. At the end of the experiment, the hamsters were assessed for testicular function in terms of the amounts of intra-testicular free testosterone (TS) and histopathological changes. RJ diet groups showed higher TS Ievels and more intensive spermatogenesis than the control group in a dose-dependent manner. The intensity of spermatogenesis and TS Ievels in the 500 ug of RJ/g diet group showed significant differences ofp < 0.01 and p < 0.05, respectively, when compared with those in the control group. These results indicate that the long-term feeding of RJ inhibits the age-associated decline in the testicular function of male hamsters.

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Section: Resultsmentioning

confidence: 99%

Effect of Royal Jelly Diet on the Testicular Function of Hamsters

Kohguchi¹,

Inoue²,

Ushio³

et al. 2004

FSTR

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“…Due to an imbalance between free-radical generation and their elimination, ROS accumulates and causes buildup of oxidative-modified proteins and a decline in cellular antioxidant defense (Harman 1981;Friguet 2006;Squier 2001). ROS formation is closely coupled to redox-active iron availability through the Haber-Weiss reaction (Leibovitz and Siegel 1980). Thus, redox-active iron enhances ROS-induced damage and turns ROS-mediated signals from prosurvival to cell death processes (Bandyopadhyay et al 1999).…”

Section: Discussionmentioning

confidence: 99%

Aging is an organ-specific process: changes in homeostasis of iron and redox proteins in the rat

Bulvik

Berenshtein

Konijn

et al. 2011

AGE

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Organ-specific changes of iron-and redoxrelated proteins occur with age in the rat. Ferritin, the major iron storage and detoxifying protein, as well as the proteins of the methionine-centered redox cycle (MCRC) were examined in old and young animals, and showed organ-dependent changes. In spleens and livers of aged rats, ferritin (protein) levels were greater than in young ones, and their iron saturation increased, rendering higher ferritin-bound iron (FtBI). Iron saturation of the ferritin molecule in the tongues and sternohyoids of old rats was lower but ferritin level was higher than in young rats, resulting in increased FtBI with age. Ferritin level in the esophagus of older rats was lower than in young rats but its molecular iron content higher thus the total FtBI remained the same. In the larynx, both ferritin and its iron content were the same in young and old animals. MCRC proteins were measured in livers and spleens only. With aging, methionine sulfoxide reductase A and B (MsrA and MsrB) levels in livers and spleens decreased. Thioredoxin1 (Trx) and Trx-reductase1 were elevated in old spleens, but reduced in livers. Aged spleens showed reduced Msr isozyme activity; but in the liver, its activity increased. mRNA changes with age were monitored and found to be organ specific. These organ-specific changes could reflect the different challenges and the selective pathways of each organ and its resultant capacity to cope with aging.

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“…ROS are produced in all tissues during aerobic metabolism and they can also be formed by photochemical reactions (Leibovitz et al 1980). ROS disturb the protective systems and thus cause lipid peroxidation and cellular damage.…”

Section: Discussionmentioning

confidence: 99%