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Presenile (early ageing) changes in tissues of Kaschin-Beck disease and its pathogenetic significance
1Institute of Basic Medicine, Liaoning Academy of Medical Sciences, Shenyang, PR, China.
Insights
Children with Kaschin-Beck disease (KBD) have lower selenium levels, leading to abnormal red blood cell membranes and cartilage. This selenium deficiency causes significant biomembrane and cartilage defects, impacting KBD pathogenesis and aging diseases.
Area of Science:
- Biochemistry
- Pathology
- Nutritional Science
Background:
- Kaschin-Beck disease (KBD) is endemic in selenium-deficient areas.
- Selenium and glutathione peroxidase activity are reduced in KBD-affected children.
- KBD is associated with abnormalities in lipid metabolism and cartilage.
Purpose of the Study:
- To investigate the impact of selenium deficiency on red blood cell membrane and cartilage in KBD.
- To elucidate the specific changes in lipid composition and structure of biomembranes in KBD patients.
- To examine alterations in cartilage metabolism, including mucopolysaccharides and collagen, in KBD.
Main Methods:
- Comparative analysis of selenium levels and glutathione peroxidase activity in children from endemic and non-endemic KBD areas.
- Biochemical analysis of red blood cell membrane components (phospholipids, cholesterol) and structure.
- Histological examination of cartilage tissue, assessing sulfation and collagen content.
- Electron microscopy to evaluate erythrocyte morphology (acanthocytes) and fragility.
Main Results:
- KBD children exhibited significantly lower selenium levels and glutathione peroxidase activity.
- Abnormalities in red blood cell membrane composition were observed, including decreased phospholipid and phosphatidylcholine, increased sphingomyelin, and altered cholesterol/phospholipid ratios.
- Increased acanthocyte content and erythrocyte fragility indicated membrane defects and damage.
- Cartilage tissue showed reduced mucopolysaccharide sulfation and increased collagen content.
- These findings suggest presenile changes in biomembranes and cartilage metabolism in KBD patients.
Conclusions:
- Selenium deficiency is a key factor in the pathogenesis of Kaschin-Beck disease.
- KBD is characterized by significant biomembrane defects and cartilage metabolic disturbances.
- The observed changes in KBD patients offer insights into the etiology of KBD and other age-related diseases.
Abstract:
The selenium level and activity of glutathione peroxidase in blood of children living in Kaschin-Beck disease (KBD) endemic areas were lower than that in nonendemic areas. KBD children were deficient in selenium, their lipid components, structure and function of the red cell membrane and cartilage tissue were abnormal. That is, the phospholipid (PL) content in the tissues of the patient was less than that of the controls in endemic and non-endemic areas. Especially as the phosphatidylcholine (PC) content decreased significantly, but sphingomyelin (SM) increased, the molar ratio of SM/PC and cholesterol (Ch)/PL increased. Increase of acanthocyte content was seen under the electron microscope and the fragility of erythrocytes was also increased. It indicated that there were membrane defects and membrane damage in KBD. At the same time, the sulfation extent of mucopolysaccharides in cartilage of patients was lower, and the collagen content was higher than that of controls. The presenile changes in lipid composition, structure and function of biomembranes and cartilage metabolism of KBD are very significant in studies on the aetiological pathogenesis of KBD and other ageing diseases.