Oxidative medicine and cellular longevity
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Oxid Med Cell Longev · Jan 2014
Antioxidant supplement inhibits skeletal muscle constitutive autophagy rather than fasting-induced autophagy in mice.
In this study, we tested the hypothesis that NAC administration leads to reduced oxidative stress and thus to decreased expression of autophagy markers in young mice. Our results reveal that NAC administration results in reduced muscle mRNA levels of several autophagy markers, including Beclin-1, Atg7, LC3, Atg9, and LAMP2. However, NAC supplement fails to block the activation of skeletal muscle autophagy in response to fasting, because fasting significantly increases the mRNA level of several autophagy markers and LC3 lipidation. ⋯ Our results clearly show that NAC administration depresses the expression of manganese superoxide dismutase (MnSOD) and TP53-induced glycolysis and apoptosis regulator (TIGAR), both of which play a predominant antioxidant role in mitochondria by reducing ROS level. In addition, we found no beneficial effect of NAC supplement on muscle mass but it can protect from muscle loss in response to fasting. Collectively, our findings indicate that ROS is required for skeletal muscle constitutive autophagy, rather than starvation-induced autophagy, and that antioxidant NAC inhibits constitutive autophagy by the regulation of mitochondrial ROS production and antioxidant capacity.
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Oxid Med Cell Longev · Jan 2014
A novel contrast-induced acute kidney injury model based on the 5/6-nephrectomy rat and nephrotoxicological evaluation of iohexol and iodixanol in vivo.
Contrast-induced acute kidney injury (CI-AKI) is a serious complication in patients after administration of iodinated contrast media. Proper animal models of CI-AKI can help understand the mechanisms involved and prevent the disorder. We used the 5/6-nephrectomized (NE) rat to develop a CI-AKI model and to evaluate differences in the toxic effects on the kidney between iohexol and iodixanol. ⋯ Iohexol and iodixanol resulted in similarly marked increases in levels of inflammation and oxidative stress. In summary, the 5/6 NE rat combined with dehydration for 48 hours is a useful pretreatment to establish a novel and reliable CI-AKI model. Iohexol induced more severe CI-AKI than iodixanol in this model.
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Oxid Med Cell Longev · Jan 2014
Propofol inhibits lipopolysaccharide-induced tumor necrosis factor-alpha expression and myocardial depression through decreasing the generation of superoxide anion in cardiomyocytes.
TNF-α has been shown to be a major factor responsible for myocardial depression in sepsis. The aim of this study was to investigate the effect of an anesthetic, propofol, on TNF-α expression in cardiomyocytes treated with LPS both in vivo and in vitro. ⋯ It is concluded that propofol abrogates LPS-induced TNF-α production and alleviates cardiac depression through gp91phox/ERK1/2 or p38 MAPK signal pathway. These findings have great clinical importance in the application of propofol for patients enduring sepsis.
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Oxid Med Cell Longev · Jan 2013
Hypothermia improves oral and gastric mucosal microvascular oxygenation during hemorrhagic shock in dogs.
Hypothermia is known to improve tissue function in different organs during physiological and pathological conditions. The aim of this study was to evaluate the effects of hypothermia on oral and gastric mucosal microvascular oxygenation (μHbO2) and perfusion (μflow) under physiological and hemorrhagic conditions. Five dogs were repeatedly anesthetized. ⋯ The improved μ HbO2 might be based on an attenuated reduction in μ flow during hemorrhage and additional hypothermia (-51 ± 21 aU) compared to hemorrhage and normothermia (-106 ± 19 aU). μDO2 was accordingly attenuated under hypothermia during hemorrhage whereas DO2 did not change. Thus, in this study hypothermia alone improves oral μHbO2 and attenuates the effects of hemorrhage on oral and gastric μ HbO2. This effect seems to be mediated by an increased μDO2 on the basis of increased μ flow.
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Oxid Med Cell Longev · Jan 2013
Malondialdehyde adduct to hemoglobin: a new marker of oxidative stress suitable for full-term and preterm neonates.
Oxidative stress may play a central role in the onset of many diseases during the neonatal period. Malondialdehyde (MDA) is a marker of lipid peroxidation. The aim of this study was to evaluate a new marker, the malondialdehyde adduct to hemoglobin (MDA-Hb), which is measured in red blood cells (RBCs) and thus does not require that an additional blood sample be drawn. ⋯ During the first months of life, MDA-Hb concentrations were 9.4 nanomol/g Hb in hospitalized preterm neonates. MDA-Hb could be used to assess oxidative stress in preterm neonates. Together with clinical variables, it could be a useful marker for oxidative stress exposition in these higher risk patients.