Galectin-3 Deficiency Reduces Cardiac and Renal Antioxidant Capacity in Mice

Galectin-3 (Gal-3) has increasingly been recognized as a modulator of inflammation, oxidative/nitrosative stress, fibrogenesis, and tissue remodeling. The objective of the current pilot study was to investigate the influence of Gal-3 on cardiac and renal antioxidant capacity using biochemical and histopathological examinations. Two groups (n=7 each) of male mice were tested: 1. control (CON) group (wild type of C57BL/6 mice) and 2. GAL-3-/- group (galectin-3-/- knockout mice). After overnight fasting, mice were sacrificed by exsanguination in ketamine (100mg/kg intraperitoneally). Then, cardiac and renal tissue samples were taken to determine the parameters of oxidative/nitrosative stress and antioxidant capacity. The levels of malondialdehyde and nitrites+nitrates was not significantly different in the GAL-3-/- group vs. the CON group. The total superoxide dismutase activity in the renal tissue of the GAL-3-/- mice was significantly lower compared to the CON group. Cardiac and renal catalase and glutathione S-transferase activity was significantly reduced in the GAL-3-/- group vs. the CON group, respectively. A significant decrease in glutathione level was also registered in hearts of the GAL-3-/- group vs. the CON group. Our findings indicate that Gal-3 deficiency does not lead to lipid peroxidation and nitrosative stress in cardiac and renal tissue in mice. However, the lack of this beta-galactoside-binding lectin does reduce antioxidant capacity in both of the investigated tissues.