[Identity and aging: psychosocial approaches]. / Concept d'identité et sujets âgés: perspectives psychosociales.

This review is devoted to the notion of identity with regard to the process of aging from various approaches in social sciences. Continuity or transformation of identity is challenged in advanced age according to the place reserved in the society for the elderly subjects and their social age groups. Study methods are discussed in relation with the theoretical models, and their relevance to address aging people singularity and influence of environment. Changes of identity among elderly subjects appear to proceed in two ways. In the first one, called "rebirth", they establish a new self. In the second way, termed "turning point", better strategy for coping the aging effects is obtained by revealing untapped dimensions of the Self.

Inactivation of stress protein p8 increases murine carbon tetrachloride hepatotoxicity via preserved CYP2E1 activity.

The p8 protein is a transcription factor that regulates the expression of genes involved in cell defense against the adverse effects of stress. Its expression is strongly, rapidly, and transiently induced in most cells on exposure to various stress agents. This study assessed the role of p8 in the response of the liver to CCl(4)-induced injury. We found that p8 was indeed overexpressed in the liver after CCl(4) administration. Hepatic injury following CCl(4) injection was monitored in wild-type and p8(-/-) mice. Serum alanine and aspartate aminotransferase activities were higher and peaked earlier in p8(-/-) mice than in wild-type mice, which is in agreement with the observation of significantly larger areas of necrosis in p8(-/-) liver. Absence of p8 expression is therefore associated with increased liver sensitivity to CCl(4). In fact, CCl(4) toxicity is mediated by derivatives generated by its conversion by the enzyme CYP2E1. It is known that CYP2E1 is downregulated in the liver during the first hours following CCl(4) administration as part of a self-defense mechanism. We found that CYP2E1 downregulation was significantly delayed in p8(-/-) liver compared with wild-type liver, allowing increased production of toxic CCl(4) derivatives. In conclusion, inactivation of the p8 gene increases liver sensitivity to CCl(4), as it appears to delay the triggering of CYP2E1 downregulation. The p8 protein is therefore an important element of hepatocyte stress response.

The post-exercise oxidative stress is depressed by acetylsalicylic acid.

In order to assess whether oxidative stress occurs after fatiguing dynamic contractions of a small forearm muscle group, we estimated the kinetics of changes in some of its biomarkers (thiobarbituric acid reactive substances or TBARS; plasma reduced ascorbic acid or RAA; erythrocyte reduced glutathione or GSH). We also tested the hypothesis that acetylsalicylic acid (ASA) may compete with endogenous radical targets, attenuating the post-exercise oxidative stress. Seven male subjects successively performed a 3-min dynamic handgrip exercise with the dominant and then the contralateral forearm. Blood samples were taken from an antecubital vein in each exercising forearm. Biochemical analyses, including the concentration measurements of lactic acid, potassium, and oxidative stress markers were performed at rest and then during the 30-min period of recovery following each exercise. The same day, exercises were repeated after ingestion of a single dose (10 mg/kg) of ASA, and the same exercises were performed after a 3-day ASA treatment (30 mg/kg/day). In control condition, the changes in TBARS, RAA and GSH were already significant immediately after the end of the forearm exercise. They culminated after 5 min, and control values were recovered by a 30-min rest period. We verified that repeated bouts failed to alter the post-exercise variations. ASA did not modify the lactic acid production significantly, though the 3-day ASA treatment significantly reduced the efflux of potassium (-74%, P < 0.05), and the post-exercise variations of TBARS (-45%, P < 0.01), RAA (-44%, P < 0.01) and GSH (-48%, P < 0.01). These results suggest that the dynamic handgrip exercise is a good model for studying the post-exercise oxidative stress and also that ASA seems to offer an efficient protection against oxidative stress and the changes in membrane permeability to potassium.