Oxidative stress and cellular and tissue damage in organogenic outbred mouse embryos after moderate perigestational alcohol intake
Tamara Anahí CollGabriela ChaufanLeticia Pérez‐TitoMartín Ricardo VentureiraCristián SobarzoMaría del Carmen Ríos de MolinaElisa Cebral
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Perigestational alcohol consumption by CF‐1 mouse, from before mating up to the period of embryo organogenesis, leads to retarded early embryo development and neural tube defects. Here, we addressed if perigestational alcohol ingestion up to Day 10 of pregnancy induces oxidative stress and changes in macromolecules and organ tissues of early organogenic embryos. Adult CF‐1 female mice were administered 10% ethanol in their drinking water for 17 days prior to mating and until Day 10 of gestation, whereas control females were administered ethanol‐free water. Our results demonstrated significantly reduced Catalase abundance and activity and increased glutathione content in the embryos of ethanol‐treated females. The nitrite level was significantly reduced, but TBARS (thiobarbituric acid reactive substances) content, an index of lipid peroxidation, did not change. Embryos derived from ethanol‐treated females also showed higher abundance of 3‐nitrotyrosine (3‐NT)‐containing proteins in all tissues, compared to the control group. Apoptosis was significantly increased in the ectoderm and mesoderm, but not in the heart—although this organ did contain more cleaved Caspase‐3‐positive cardiomyocytes per area of ventricular myocardium than controls. In sum, moderate perigestational alcohol ingestion up to Day 10 of gestation in mice induces oxidative stress by altering radical nitrogen species and antioxidant enzymatic and non‐enzymatic mechanisms in embryos. Further, generalized protein nitration, due to unbalanced nitric oxide levels associated with tissue‐specific apoptosis, was detected in embryos, suggesting that oxidative mechanisms may play an important role in the perigestational alcohol‐induced malformation of organogenic embryos exposed to ethanol.Keywords:
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Summary: Plasma concentrations of thiobarbituric acid reactive substances (TBARS) are an index of lipid peroxidation and oxidative stress. The protocol describes how the DiaComp quantitates TBARS in the animal models. Diabetic Complication:
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Lipid peroxidation products, both lipid hydroperoxides and thiobarbituric acid reactive substances (TBARS) were determined in the plasma of 31 uremic patients treated with maintenance hemodialysis. Whereas patients had significantly elevated TBARS compared to 93 healthy controls (4.25 ± 1.53 vs. 1.66 ± 0.50 μmol/l; p < 0.01) lipid hydroperoxides were not detected in the plasma of patients before dialysis. After hemodialysis, a slight increase in TBARS was observed (4.50 ± 1.97 μmol/l, p > 0.01). However, when the TBARS were corrected for hemoconcentration by relating TBARS to the plasma cholesterol concentrations a statistically significant decrease of TBARS was observed (1.02 ± 0.63 μmol TBARS/mmol cholesterol vs. 0.84 ± 0.60 μmol TBARS/mmol cholesterol; p < 0.01) after 240 min of hemodialysis. There was no evidence for the formation of plasma lipid hydroperoxides in the extracorporeal circulation. It is therefore suggested that elevated TBARS in chronic renal failure are not caused by the dialysis therapy.
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When measuring endogenous TBARS levels from tissues of animals(in vitro)the presence of exogenous antioxidants in the tissue is likely to interfere with the TBARS assay to give artificially low values.Such low values do not then reflect protection against peroxidation in vlvo.The type and extent of the reduction in TBARS values depend on the TBARS assay conditions.Firstly there appears to be an initial(probably iron induced) burst of peroxidtion uring homogenisation,which is antiosidant susceptible.In addition added TBARS products are formed during the final heating stage in methods which retain membrane bound reactants throughout the assay,and this step is also suceptible to antioxidant presence.
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Nitric oxide is a physiological regulator of endothelial function and hemodynamics. Oxidized products of nitric oxide can form nitrotyrosine, which is a marker of nitrative stress. Cigarette smoking decreases exhaled nitric oxide, and the underlying mechanism may be important in the cardiovascular toxicity of smoking. Even so, it is unclear if this effect results from decreased nitric oxide production or increased oxidative degradation of nitric oxide to reactive nitrating species. These two processes would be expected to have opposite effects on nitrotyrosine levels, a marker of nitrative stress.In this study, we evaluated associations of cigarette smoking and chronic obstructive pulmonary disease (COPD) with nitrotyrosine modifications of specific plasma proteins to gain insight into the processes regulating nitrotyrosine formation.A custom antibody microarray platform was developed to analyze the levels of 3-nitrotyrosine modifications on 24 proteins in plasma. In a cross-sectional study, plasma samples from 458 individuals were analyzed.Average nitrotyrosine levels in plasma proteins were consistently lower in smokers and former smokers than in never smokers but increased in smokers with COPD compared with smokers who had normal lung-function tests.Smoking is associated with a broad decrease in 3-nitrotyrosine levels of plasma proteins, consistent with an inhibitory effect of cigarette smoke on endothelial nitric oxide production. In contrast, we observed higher nitrotyrosine levels in smokers with COPD than in smokers without COPD. This finding is consistent with increased nitration associated with inflammatory processes. This study provides insight into a mechanism through which smoking could induce endothelial dysfunction and increase the risk of cardiovascular disease.
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