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3.8 - 2nd July 1998


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Caloric intake alters the efficiency of catalase mRNA translation in the liver of old female mice.

Dhahbi JM, Tillman JB, Cao S, Mote PL, Walford RL, Spindler SR

Department of Biochemistry, University of California, Riverside, USA.

J Gerontol A Biol Sci Med Sci 1998 May;53(3):B180-B185

The free radical theory of aging predicts that calorie restriction, which extends life span, should reduce oxidant damage. In mammals, the oxidative processes centered in the liver are a major source of free radicals. Liver catalase has the dominant role in the intracellular detoxification of hydrogen peroxide. In male rodents, published studies indicate that aging decreases catalase gene transcription and that calorie restriction obviates this effect. In females, published studies are inconsistent, and no molecular mechanisms have been identified. Here we report that, in female mice, aging can lead to an increase in the translational efficiency of hepatic catalase mRNA, and that calorie restriction obviates this effect. Consideration of these results and published studies leads us to propose that the variability in catalase results in females may arise from the small number of studies or from unique aspects of female physiology, perhaps the estrous cycle and its cessation with age.

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The rate of free radical production as a determinant of the rate of aging: evidence from the comparative approach.

Perez-Campo R, Lopez-Torres M, Cadenas S, Rojas C, Barja G

Departamento de Fisiologia Animal, Facultad de Biologia, Universidad Complutense, Madrid, Spain.

J Comp Physiol [B] 1998 Apr;168(3):149-158

The relationship of oxidative stress with maximum life span (MLSP) in different vertebrate species is reviewed. In all animal groups the endogenous levels of enzymatic and non-enzymatic antioxidants in tissues negatively correlate with MLSP and the most longevous animals studied in each group, pigeon or man, show the minimum levels of antioxidants. A possible evolutionary reason for this is that longevous animals produce oxygen radicals at a low rate. This has been analysed at the place where more than 90% of oxygen is consumed in the cell, the mitochondria. All available work agrees that, across species, the longer the life span, the lower the rate of mitochondrial oxygen radical production. This is true even in animal groups that do not conform to the rate of living theory of aging, such as birds. Birds have low rates of mitochondrial oxygen radical production, frequently due to a low free radical leak in their respiratory chain. Possibly the low rate of mitochondrial oxygen radical production of longevous species can decrease oxidative damage at targets important for aging (like mitochondrial DNA) that are situated near the places of free radical generation. A low rate of free radical production can contribute to a low aging rate both in animals that conform to the rate of living (metabolic) theory of aging and in animals with exceptional longevities, like birds and primates. Available research indicates there are at least two main characteristics of longevous species: a high rate of DNA repair together with a low rate of free radical production near DNA. Simultaneous consideration of these two characteristics can explain part of the quantitative differences in longevity between animal species.

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Aminoguanidine prevents age-related arterial stiffening and cardiac hypertrophy.

Corman B, Duriez M, Poitevin P, Heudes D, Bruneval P, Tedgui A, Levy BI

Service de Biologie Cellulaire, Commissariat a l'Energie Atomique, Centre d'Etudes de Saclay, Gif sur Yvette, 91191 Cedex, France.

Proc Natl Acad Sci U S A 1998 Feb 3;95(3):1301-1306

Aging is associated with cardiac hypertrophy and arterial stiffening possibly associated with accumulation of advanced glycation end products (AGEs). We evaluated the effect of aminoguanidine, an inhibitor of AGE production, on end-stage alterations of renal and cardiovascular systems. Normotensive WAG/Rij rats were treated from 24 to 30 mo with aminoguanidine and compared with a control group. Aminoguanidine did not modify body and kidney weights but prevented the age-related cardiac hypertrophy (heart weight: 1276 +/- 28 mg and 1896 +/- 87 mg in 24- and 30-mo-old control animals and 1267 +/- 60 mg in 30-mo-old treated rats, P < 0.01). The increase in mesangial surface in aging rats was reduced by 30% by aminoguanidine. Collagen content of the arterial wall increased between 24 and 30 mo whereas elastin content, media thickness, and smooth muscle cell number remained unchanged. Aminoguanidine did not affect these parameters; however, the age-related increase in aortic impedance (12.4 +/- 1.4 and 18.2 +/- 1.9 10(3).dyne.sec.cm-5 in control 24- and 30-mo-old rats, P < 0.01) and the decrease in carotid distensibility (0.79 +/- 0.11 and 0.34 +/- 0. 07 mm Hg-1 in control 24- and 30-mo-old rats, P < 0.01) were prevented by aminoguanidine. The prevention of arterial stiffening and cardiac hypertrophy in the absence of changes in collagen and elastin content suggests that the effect of aminoguanidine is related to a decrease in the AGE-induced cross-linking of the extracellular matrix.

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