Psychological stress is associated with increased oxidative stress, a pro-inflammatory state, increased rate of infection, and cardiovascular disease. Cardiovascular disease also is associated with increased stress, homocysteine, and C-reactive protein (CRP) levels. In this study, the authors measured various markers of psychological stress and correlated with homocysteine, CRP, salivary IgA, and oxidative stress. The results of the study showed that psychological stress is associated with pro-oxidant and pro-inflammatory states as evidenced by either decreased NT levels and/or increased CRP concentrations. Conversely, positive or low stress parameters, indicating good life skill mechanisms were associated with increased NT and decreased CRP--indications of a low pro-oxidant state. Homocysteine was associated with increased anger (anger-suppression and anger-experience), psychological parameters associated with cardiovascular disease and also mildly elevated CRP and homocysteine levels. Psychological well-being and stress are correlated with biochemical parameters both positively and negatively in relation to immunity and cardiovascular disease processes. The cross-sectional design and correlational approach used in this study preclude any inferences of causality but suggest several potentially useful avenues for future research.
Vasopressin induced a transient increase of 50% in the total concentration of diacylglycerols (determined by g.l.c.) in isolated hepatocytes. The increase was maximal at 0.25 min, and the concentration of diacylglycerols in cells treated with vasopressin had returned to the basal value by 4 min. No change in the concentration of diacylglycerols was observed after the treatment of cells with glucagon. The dependency of this effect on the concentration of vasopressin was similar to that of the effect of the hormone on 45Ca2+ efflux measured at 0.1 mM extracellular Ca2+. Vasopressin increased the proportion of arachidonic acid and stearic acid and decreased the proportion of oleic acid present in the diacylglycerols. In hepatocytes prelabelled with [14C]arachidonic acid, vasopressin increased the amount of [14C]diacylglycerol. The effects of vasopressin on the total concentration of diacylglycerols and [14C]diacylglycerol were mimicked by an exogenous phospholipid phosphodiesterase (phospholipase C) from Clostridium perfringens. The results are consistent with the conclusion that the transient increase in diacylglycerols induced by vasopressin is caused by the rapid hydrolysis of both the phosphoinositides and one or more other phospholipids.
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