Human cathepsin D.

A literature survey was performed of human cathepsin D gene, cathepsin D biosynthesis, posttranslatory modifications, transport within the cell, substrate specificity and catalytic effect. Methods used to determine the activity and level of this proteinase as well as its role in the biochemistry and pathobiochemistry of cells, tissues and organs were considered

Regulatory role of cathepsin D in apoptosis.

Cathepsin D (CTSD, EC 3.4.23.5) is well known aspartyl protease. Among different role in cell physiology, a new function of this enzyme is examined. Cathepsin D is an important regulator of apoptotic pathways in cells. It acts at different stage of intrinsic and extrinsic pathway of apoptosis. Cathepsin D can either induce apoptosis in presence of cytotoxic factors, but in certain studies an inhibitory role in apoptosis was also reviewed. Detailed review of involvement of cathepsin D in cell apoptosis is a purpose of this paper

Role of cathepsin A and cathepsin C in the regulation of glycosidase activity

Increased tissue activity of cathepsin A and cathepsin C can be observed in many pathological conditions. It is associated with an enhanced degradation of glycosaminoglycans, proteoglycans, and glycoproteins, and results in their decreased tissue content. Cathepsin C releases the glycosidases from complexes formed with cathepsin A, and reinstates their activity. In this review a current state of knowledge is presented concerning the regulation of selected glycosidases activity by cathepsin A (EC 3.4.16.1) and C (EC 3.4.14.1)

Rare genotype del2,3/2184insA in a cystic fibrosis patient.

In this paper we present an interesting case of cystic fibrosis patient with rare genotype de12,3/2184insA and atypical clinical image including: mild symptoms in an early phase of disease, quick progress of lung disease, complicated with pneumothorax after Bordetella pertussis infection and very good response to systemic and inhaled steroid therapy

Regulatory role of cathepsin D in apoptosis.

Cathepsin D (CTSD, EC 3.4.23.5) is well known aspartyl protease. Among different role in cell physiology, a new function of this enzyme is examined. Cathepsin D is an important regulator of apoptotic pathways in cells. It acts at different stage of intrinsic and extrinsic pathway of apoptosis. Cathepsin D can either induce apoptosis in presence of cytotoxic factors, but in certain studies an inhibitory role in apoptosis was also reviewed. Detailed review of involvement of cathepsin D in cell apoptosis is a purpose of this paper

Salivary lysozyme in smoking alcohol dependent persons

The purpose of the study was evaluation the effect of chronic alcohol intoxication and smoking, on the concentration and output of salivary lysozyme. In the study participated 37 persons, consisted of 17 male smoking patients after chronic alcohol intoxication (AS), and 20 control nonsmoking male social drinkers (CNS) with no history of alcohol abuse or smoking. For all participants the DMFT index (decayed, missing, or filled teeth), gingival index (GI) and papilla bleeding index (PBI) were assessed. Resting whole saliva was collected 24 to 48 hours after chronic alcohol intoxication period. Level of lysozyme was assessed by radial immunodiffusion method. The differences between groups were evaluated using Mann-Whitney “U” test. Salivary flow (SF) was significantly lower in smoking alcohol dependent persons than in the control group. It was found a tendency to increase in the concentration of lysozyme and significantly lower lysozyme output in smoking persons chronically intoxicated by alcohol, as compared to the control group. Gingival index was significantly higher in smoking alcohol dependent persons than in the control group, whereas there were no significant differences in PBI and DMFT indexes between these groups. There were no significant correlations between the amount/number and length of alcohol consumption as well as cigarette smoking, and the concentration as well as the output of lysozyme. There were also no significant correlations between salivary lysozyme output/concentration and SF. In conclusion, reduced salivary flow and salivary lysozyme output may impair innate immunity of the oral cavity. Reduced levels of salivary flow and salivary lysozyme output seem to be more likely to be the result of ethanol action than smoking. We confirmed that persons addicted to alcohol and cigarettes have worse periodontal condition than general population, which partially may be due to the decreased protective effect of reduced salivary flow and lysozyme output

Alcohol abuse and glycoconjugate metabolism

The relationship between alcohol consumption and glycoconjugate metabolism is complex and multidimensional. This review summarizes the advances in basic and clinical research on the molecular and cellular events involved in the metabolic effects of alcohol on glycoconjugates (glycoproteins, glycolipids, and proteoglycans). We summarize the action of ethanol, acetaldehyde, reactive oxygen species (ROS), nonoxidative metabolite of alcohol — fatty acid ethyl esters (FAEEs), and the ethanol-water competition mechanism, on glycoconjugate biosynthesis, modification, transport and secretion, as well as on elimination and catabolism processes. As the majority of changes in the cellular metabolism of glycoconjugates are generally ascribed to alterations in synthesis, transport, glycosylation and secretion, the degradation and elimination processes, of which the former occurs also in extracellular matrix, seem to be underappreciated. The pathomechanisms are additionally complicated by the fact that the effect of alcohol intoxication on the glycoconjugate metabolism depends not only on the duration of ethanol exposure, but also demonstrates dose- and regional-sensitivity. Further research is needed to bridge the gap in transdisciplinary research and enhance our understanding of alcohol- and glycoconjugate-related diseases