Influence of beta-galactose-specific mitochondrial lectins from prostate hyperplasic tissue on mitochondrial properties

Abstract

Galactose-specific lectins (Gal-lectins) were isolated from the mitochondrial fraction of prostate post-operational hyperplasic tissue of two diagnoses: benign prostate hyperplasic tissue with low-grade intraepithelial neoplasia (LGPIN) and benign prostate hyperplasic tissue with atypical adenomatous hyperplasia (AAH). They had similar molecular weight and other properties. Effects of these lectins were investigated in vitro model experiments on bovine liver cells mitochondrial properties. Time-dependent changes: (i) in the amount of H₂O₂; (ii) redox state of Cu in cytochrome oxidase and (iii) redox state of heme in cytochrome a+a₃ (cyt a+a₃) of cytochrome c oxidase complex were studied. Gal-lectins from both sources increase the amount of H₂O₂ and decrease the redox state of Cu in cytochrome oxidase and heme in cyt a+a₃. However the Gallectin from tissue with more severed transformation (AAH) expresses significantly more strong and long-lasting influence. These effects are mediated by galactose binding domain of the lectins as are completely abolished by the inclusion of galactose in reaction medium. Accumulation of H₂O₂ and long-lasting decrease in the redox state of key enzymes of mitochondrial respiration chain could induce defective functioning of these organelles and whole cells. Obtained data point the possible way, which enhances further transformation of prostate tissue by release of Gallectins from damaged mitochondria.

Key Words::

• benign prostatic hyperplasia
• prostatic neoplasms
• adenosis
• mitochondrial electron transport
• oxygen radical
• animal lectins

Declaration of interest: The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.