engleski

Psychological stress acts at the molecular level

Under stress human organism redistributes its energy resources in the anticipation of an incoming threat. Systems which are needed for the immediate reaction (locomotory and sensory) are activated to their full extent, while secondary systems (digestive, immune, reproductive, etc.) are temporarily depressed. Damages to depressed systems are inevitable in prolonged stress, and a number of epidemiological and experimental studies conducted during the past years clearly demonstrated its effects on development and course of many diseases. However, biochemical basis for these effects is still mostly unknown. Glycosylation, as the most important posttranslational modification and integrating mechanisms, appears to be significantly involved in the stress response. First indications that glycosylation might play some role in the stress response we found when we analyzed glycoproteins in serum of prisoners released from Serbian concentration camps [1]. Among other changes, the most interesting was the appearance of a novel glycoprotein which we subsequently named Stressin. Using MALDI-MS we determined exact masses of its glycosylated and deglycosylated tryptic fragments, and by comparing them to computer databases confirmed that Stressin is a novel protein. Analysis of its glycosylation revealed a surprising extent of N-linked oligosaccharides amounting to over 40% of the total mass. Neuraminidase digestion revealed that 3, 6 kDa of the mass originated from 12 sialic acid moieties [2]. Interaction with lectin receptors is one of the main modes of glycoconjugate action, and indeed, we have found several changes in lectins on animal models of stress. Stress induced expression of a novel lectin CBP33, and in the same time it affected interaction of CBP35 and CBP67, most probably through carbohydrate-lectin interactions [3]. Glycosyltransferases, particularly sialyltransferases (ST) are also prone to changes in stress and appear to be under direct control of steroid hormones. Adrenalectomy significantly decreases ST activity in the brain, but in the same time it increases ST activity in the liver. While exogenous corticosteroids can restore normal ST activity in the brain, liver ST appears to be regulated by different mechanisms. Hopefully we will be able to specifically influence some of these processes in the future, and thus provide better targets for pharmacological therapy.

Stress; Biochemistry; Glycobiology

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