Taurine supplementation protects lens against glutathione depletion.

OBJECTIVE: Cataract which is defined as opacification of eye lens forms approximately 40% of total blindness causes all through the world. Age is the biggest risk factor for cataracts and oxidative stress is known to be one of the most important factors causing cataract formation. Age-related nuclear cataract (ARN) is associated with a loss of glutathione in the center of the lens. Taurine is an important antioxidant in lens tissue. Although, there is a high amount of taurine in lenses in early life, its concentration declines with age. In this study, we aimed to investigate the effects of supplemental taurine in lens tissues in an in vivo oxidative stress model which is induced by glutathione depletion to mimic ARN. MATERIALS AND METHODS: Glutathione depletion was induced in rabbits subcutaneously with l-Buthionine -(S,R)-sulfoximine (BSO)- a glutathione inhibitor and the rabbits were treated with taurine. Total GSH, reduced GSH, GSH/GSSG ratio and MDA levels were measured. RESULTS: BSO lowered the reduced GSH and total GSH levels and GSH/GSSG ratio. Taurine reversed these effects. On the other hand, BSO enhanced MDA level which is normalized by taurine. CONCLUSIONS: These findings suggest that glutathione depletion with BSO may be a useful model to mimic ARN and dietary intake of taurine, may have an important role in decelerating the process of cataract formation.

Diverse effects of taurine on vascular response and inflammation in GSH depletion model in rabbits.

OBJECTIVE: A reduction in GSH and an increase in free radicals are observed in inflammatory diseases, indicating oxidative stress. Taurine protects cells from the cytotoxic effects of inflammation. There have been limited studies to date evaluating the effect of taurine in oxidative stress-induced vascular dysfunction and its role in vascular inflammatory diseases. Therefore, we aimed to investigate the effect of taurine on the regulation of vascular tonus and vascular inflammatory markers in rabbit aortae and carotid arteries in oxidative stress-induced by GSH depletion. MATERIALS AND METHODS: Rabbits were treated subcutaneously with buthionine sulfoximine (BSO), GSH-depleting compound and/or taurine. Cumulative concentration-response curves for acetylcholine (ACh), phenylephrine and 5-hydroxytriptamine (5-HT) were constructed with or without Nω-nitro-L-arginine (LNA) in the carotid artery and aorta rings. Immunohistochemical staining was performed for TNF-α and IL-1ß. RESULTS: BSO increased ACh-induced NO-dependent relaxations, phenylephrine-induced contractions in the carotid artery and 5-HT induced-contractions in both the carotid artery and the aorta. BSO decreased EDHF dependent relaxations only in the aorta. ACh-induced NO-dependent relaxations and augmented contractions were normalized by taurine. BSO increased TNF-α expressions in both carotid arteries and aortas, which were reversed by taurine. The BSO-induced increase in IL-1ß was reversed by taurine only in aortae. CONCLUSIONS: Treatment with BSO resulted in vascular reactivity changes and increased immunostaining of TNF-α in mainly carotid arteries in this model of oxidative stress. The effect of taurine on BSO-induced vascular reactivity changes varied depending on the vessel. The inhibition of the increase in TNF-α expression by taurine in both carotid arteries and aortae supports the proposal that taurine has a beneficial effect in the treatment of inflammatory diseases such as atherosclerosis.

Taurine suppresses oxidative stress-potentiated expression of lectin-like oxidized low-density lipoprotein receptor and restenosis in balloon-injured rabbit iliac artery.

1. In endothelial cells, the major receptor for the binding and internalization of oxidized low-density lipoprotein (LDL) is the lectin-like oxidized LDL receptor (LOX-1). The aim of the present study was to investigate the effects of taurine on intimal thickening and LOX-1 expression under normal and oxidative conditions. 2. The iliac artery of rabbits were subjected to balloon injury and oxidative stress was induced by 14 days treatment of rabbits with 75 mg/kg, s.c., buthionine sulfoximine (BSO), a specific inhibitor of glutathione synthesis. Taurine was administered in drinking water (1%, w/v) for 14 days in the presence (BSO + Taurine group) and in the absence of BSO treatment (Taurine group). In taurine and placebo groups, rabbits were injected with 4 mL, s.c., 0.9% NaCl (vehicle for BSO) for 14 days. 3. Taurine (1% in drinking water, w/v) preserved plasma levels of anti-oxidants and lowered the increased blood pressure induced by BSO. The stenosis rate of 29.92% in the placebo group increased to 72.20% in the BSO group, which was significantly reduced to 42.21% by taurine (P < 0.001; n = 5). Localization of LOX-1 to the intima and media of the iliac artery was demonstrated in the present study. Taurine treatment reduced the BSO-induced increase in LOX-1 expression at both the protein and mRNA levels (P < 0.05 and P < 0.01, respectively). 4. The results demonstrate that the stenosis rate and LOX-1 expression correlate well with oxidative status. Manipulation of LOX-1 expression by taurine may have therapeutic benefits in preventing restenosis.

Telomeric restriction analysis of vascular smooth muscle cells following balloon angioplasty in rabbits.

Intimal hyperplasia due to smooth muscle cell proliferation and migration has been reported to be responsible for the pathogenesis of atherosclerosis and restenosis, manifested following balloon angioplasty. In this study, we employed the balloon angioplasty model to study telomere length regulation in proliferating vascular smooth muscle cells. Our results showed that balloon angioplasty in iliac arteries resulted in intimal hyperplasia due to proliferation of the smooth muscle cells and small size telomeric restrictional fragments were evident in injured arteries.