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The calpain-1-activated apoptotic pathway plays a key role in right ventricular hypertrophy (RVH). Taurine has been shown to attenuate apoptosis by inhibiting calpain activity. This experiment aimed to determine whether taurine could prevent RVH by inhibiting the calpain-1/cytochrome c apoptotic pathway. The broilers were given 1% taurine dissolved in drinking water and were raised at 10 °C ~ 12 °C from day 21 to day 42. At 21 d, 28 d, 35 d and 42 d, the right ventricular (RV) tissues were collected. Increased RVH index, angiotensin II, norepinephrine and atrial natriuretic peptide mRNA expression were reduced by taurine in the broiler RVs. Taurine obviously inhibited cardiomyocyte apoptosis via maintaining the mitochondrial membrane potential and decreased the activation of caspase-9 and caspase-3 in the broiler RVs. The antioxidant assay demonstrated that taurine enhanced the activities of superoxide dismutase, total antioxidant capacity and glutathione peroxidase and the glutathione/glutathione disulfide ratio. Western blot results revealed that taurine also downregulated the expression of calpain-1 and cytosolic cytochrome c while upregulating the expression of Bcl-2/Bax and mitochondrial cytochrome c in broiler cardiomyocytes during RVH. In summary, we found that taurine could enhance cardiomyocyte antioxidant ability and further prevented cardiomyocyte apoptosis by inhibiting the calpain-1/cytochrome c pathway during RVH in broilers.

In males, the decline of androgen synthesis, spermatogenesis and sexual function are the main phenotypes of aging, which may be attributed to testicular dysfunction. Taurine can act as an antioxidant, a testosterone secretion stimulator, a sperm membrane stabilizer and motility factor, and an anti-apoptotic agent. Recent observational studies suggested that taurine may play an important role in spermatogenesis, but to date whether taurine has anti-aging effects on testes remains unknown. We found that in aged rats testicular SDH and G6PDH activities, marker enzymes of testes, serum testosterone, testicular 3β-HSD and 17β-HSD mRNA expression levels were significantly increased by taurine treatment. Taurine administration also markedly raised the sperm count, viability and motility, decreased the sperm abnormality. Our data suggested that taurine can postpone testicular function deterioration in aged rats. Importantly, we observed obvious elevation of testicular antioxidant enzymes (SOD, GSH, GSH-Px) activities, and remarkable reduction of ROS and MDA by taurine administration, indicating taurine can decrease testicular oxidative stress and lipid peroxidation in aged rats. Finally, we found taurine effectively reduced testicular DNA fragmentation, increased testicular Bcl-2 protein expression, and decreased cytochrome c, Bax, Fas, FasL and caspase-3 expression, suggesting taurine can prohibit aged testicular apoptosis by mitochondrial dependent and independent signal pathway. In summary, our results indicated that taurine can suppress testicular function deterioration by increasing antioxidant ability and inhibiting apoptosis.

One pathogenic mechanism of ethanol-induced liver injury is the excessive production of reactive oxygen species (ROS), which may result in alcoholic liver disease (ALD) characterized by cell death due to necrosis and apoptosis. Taurine was proved to protect against liver damage. However, whether taurine attenuates ethanol-induced hepatic apoptosis remains unknown. The present study aims to elucidate this effect and its underlying mechanism. Taurine was administered to ALD rats and an in vitro experiment in which taurine was added to primary rat hepatocytes cultured with ethanol was conducted. Mitochondrial function and anti-oxidative capacity of the liver were tested. TUNEL and AO-EB double staining were conducted to detect apoptosis of liver cells. Expressions of factors and proteins involved in mitochondrial and death receptor pathways were detected by RT-PCR and Western-blot. The results showed that taurine inhibited the decline of cell functions and apoptosis in hepatocytes cultured with ethanol. Furthermore, increased malondialdehyde (MDA) and reduced superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), total antioxidant capacity (T-AOC), cytochrome c oxidase (COX) and NADH dehydrogenase (ND) in ALD rats were mediated by taurine. RT-PCR and western-blot results revealed that taurine down-regulated expression of Bax, Fas, Fas ligand (FasL), caspase 3 and caspase 9 while up-regulating the expression of Bcl-2 in ethanol-cultured hepatocytes. In summary, taurine inhibit ethanol-induced hepatic apoptosis by regulating mitochondrial or death receptor pathways.

To investigate the effect of taurine on alcoholic liver disease in rats, male Wistar rats were administered alcohol intragastrically for 3 months. The effect of beta-alanine-mediated taurine depletion and taurine administration on the development of alcoholic liver disease was examined. It was found that taurine administration produced lower levels of aspartate aminotransferase and alkaline aminotransferase than that of the untreated group. In addition, the levels of hepatic total protein, glutathione and superoxide dismutase were higher in the taurine treated groups than those in the untreated control or the taurine depleted groups, while hepatic malondialdehyde content exhibited the negative effect. Moreover, the concentrations of hepatic hydroxyproline, serum hyaluronic acid, interleukin-2, interleukin-6, tumor necrosis factor-alpha and laminin were all decreased in the taurine treated groups. The pathological changes showed that the percentage of fatty degeneration and inflammation in the taurine groups were lower than that of the control, taurine depleted and automatic recovery groups. These in vivo findings demonstrate that hepatic disease caused by chronic alcohol consumption can be prevented and cured by administration of taurine.