Numerous experimental and several clinical studies demonstrated that taurine (2-aminoethanesulfonic acid) helps the cardiovascular system through a variety of mechanisms including modulation of intracellular calcium concentration, antagonism of angiotensin II action, membrane-stabilizing, antioxidant, and lipid-lowering effects. The aim of the study was to assess the effects of taurine (T) on mitochondrial functions and oxidative stress in the heart from rats with type 2 diabetes.

Type 2 diabetes was induced in male Wistar rats by a single intraperitoneal injection of 50mg/kg streptozotocin followed by a high-fat diet during four weeks. All animals were divided into three groups: intact (control) group (C, n=8), untreated diabetic group (D, n=8) and diabetic rats treated with T (D+T, n=8) for 8 weeks (100mg/kg/day per os) after diabetes induction. The activities of mitochondrial respiratory enzymes cytochrome c oxidase, succinate dehydrogenase and aconitase were measured. Levels of reactive oxygen species (ROS), reduced glutathione (GSH) and antioxidant enzymes glutathione-reductase (GSSG-reductase), glutathione peroxidase (GSH-Px), manganese superoxide dismutase (Mn-SOD) activities were determined as biomarkers of oxidative stress in mitochondrial preparations.

A significant increase in ROS production (D: 0.38±0.04 vs. 0.17±0.02nmol H2O2/min/mg of protein, P<0.01) was accompanied by 2-fold reduction of GSH level and compensatory elevation of antioxidant enzymes GSSG-reductase (D: 6.02±0.28 vs. 4.42±0.29μmol/min/mg protein, P<0.05), GSH-Px (D: 28.01±3.22 vs. C: 11.32±1.12μmol/min/mg protein, P<0.01), Mn-SOD (D: 29.49±1.94 vs. C: 16.97±1.10U/mg protein, P<0.02) activities in diabetic heart mitochondria. In addition, mitochondrial matrix aconitase, a ROS sensitive enzyme, was inhibited by 50% in the diabetic rat heart. The activities of mitochondrial respiratory enzymes succinate dehydrogenase (complex II) were significantly decreased (D: 14.65±1.13 vs. C: 23.70±2.04nmol/min/mg protein, P<0.02), while that of cytochrome c oxidase (complex IV) were not changed in diabetic rats in comparison with intact animals. Administration of T provided reduction in ROS production (D+T: 0.14±0.02nmol H2O2/min/mg of protein, P<0.01), GSH-Px (D+T: 13.22±1.42μmol/min/mg protein, P<0.02), Mn-SOD (D+T: 17.35±1.24U/mg protein, P<0.02) activities and increased GSH level (D+T: 5.75±0.31 vs. D: 2.89±0.29nmol/mg of protein, P<0.05) and aconitase activity (D+T: 312.2±29.3 vs. D: 138.5±13.5nmol/min/mg of protein, P<0.01) in heart mitochondria compared to diabetic control group. In addition, T also normalised succinate dehydrogenase activity in heart mitochondria of diabetic rats.

These data demonstrate that taurine can protect against mitochondrial dysfunction and oxidative stress in the heart of diabetic rats. Thus, this action of taurine could be an important mechanism for providing benefits to the cardiovascular system in patients with type 2 diabetes.