Oral nitrate therapy does not affect glucose metabolism in healthy men

• 1 Previously, we demonstrated that nitric oxide (NO) may be an important mediator of peripheral glucose disposal. The aim of the present study was to determine whether acute oral nitrate therapy improves glucose metabolism in healthy individuals.
• 2 Healthy men (n = 10), aged between 19 and 46 years, participated in a randomized cross‐over placebo‐controlled study. During Visit 1, participants received a dose‐graded intravenous infusion of sodium nitroprusside (SNP; titrated from a dose of 0.5 μg/kg per min to a maximum of 2 μg/kg per min and delivered at a rate of 2 mL/min over 30 min). On Visits 2, 3 and 4, participants received oral extended‐release isosorbide mononitrate (120 mg), pentaerythritol tetranitrate (160 mg) and placebo in a randomized Latin square design (one treatment per visit). The main outcome measures were plasma glucose and insulin levels and glucose tolerance determined by an oral glucose tolerance test following the SNP infusion and 3 h after nitrate/placebo administration. Exhaled NO, cGMP and pulmonary blood flow were also measured for 3 h after administration of nitrate/placebo and after SNP infusion.
• 3 None of the nitrate interventions influenced measures of glucose metabolism. Following SNP infusion, there was no change in plasma glucose (P = 0.42) or insulin (P = 0.25) levels, and the response to a glucose load did not different from baseline (P = 0.46). Similarly, neither of the oral nitrates altered plasma glucose (P = 0.24) or insulin levels (P = 0.90) or glucose tolerance (P = 0.56) compared with placebo.
• 4 In conclusion, these results indicate that acute oral nitrate therapy does not influence glucose metabolism. Studies using NO donors in a chronic setting are required to clarify the role of NO in mediating peripheral glucose uptake.

     

A high intake of conjugated linoleic acid does not affect liver and kidney function tests in healthy human subjects

Conjugated linoleic acid (CLA) is consumed widely as a supplement. It causes hepatomegaly in animals, but toxicological data in humans are limited. We therefore studied the effect of a high daily intake of CLA on liver and kidney function in healthy subjects. Twenty subjects received 14.6 g cis-9,trans-11 CLA and 4.7 g trans-10,cis-12 CLA isomers a day for 3 weeks. Liver and kidney function was measured at 0, 3, 7, 10, 16, and 21 days. Mean values of all tests remained within normal limits. Lactate dehydrogenase (mean ± SD) increased from 290.9 ± 43.6 to 322.5 ± 60.7 U/L (p = 0.04) on day 21. One subject exceeded the upper limit of normal of 450 U/L on day 21, to 472 U/L and another showed an isolated elevation to 555 U/L on day 7. γ-Glutamyltranspeptidase increased from 12.1 ± 5.9 to 13.5 ± 6.2 U/L (p = 0.002). No one exceeded the upper limit of 50 U/L for men and 40 U/L for women. A daily intake of 19.3 g CLA for 3 weeks does not produce clinically relevant effects on markers of liver and kidney function in healthy volunteers.     

硫辛酸联合缬沙坦治疗早期糖尿病肾病的疗效及其对氧化应激的影响

目的观察硫辛酸联合缬沙坦对早期糖尿病肾病的疗效及对其氧化应激的影响。方法将120例早期糖尿病肾病患者按数字表法随机分成两组,每组60例。A组予缬沙坦80m∥次、每天1次口服;B组予缬沙坦80mg／次、每天1次口服,同时予硫辛酸每天600mg静脉滴注治疗。两组疗程均为2周。比较两组治疗前后24h尿微量白蛋白排泄率（24hUAER）、血清超氧化物歧化酶（SOD）、血清丙二醛（MDA）、血清谷胱甘肽过氧化物酶（GSH-PX）、总抗氧化能力（T—AOC）。结果治疗前A组24hUAER、SOD、MDA、GSH．PX、T．AOC分另U为（153．354-12．78）mg／d、（82．24±10．23）U／mL、（5．02±0．24）μmol／L、（71．58±9．22）U、（7．254-1．26）U／mL,治疗后分别为（128．85±11．62）mg／d、（83．04±10．36）U／mL、（4．98±0．23）I~mol／L、（72．24±9．18）U、（7．29±1．32）U／mL,其中治疗前后24hUAER差异有统计学意义（￡=2．285,P〈0．05）。治疗前B组24hUAER、SOD、MDA、GSH—PX、T-AOC分别为（153．18±12．65）mg／d、（82．25±10．24）U／mL、（5．0l-t-O．24）txmol／L、（71．60±9．21）U、（7．25±1．22）U／mL,治疗后分别为（106．54±10．82）mg／d、（91．35±11．53）U／mL、（4．21±0．18）izmol／L、（80．25±9．88）U、（8．76±1．70）U／mL,治疗前后差异均有统计学意义（t=2．757、2．523、2．748、2．652、2．644,均P〈0．05）。治疗后B组24hUAER、SOD、MDA、GSH—PX、T．AOC与A组差异均有统计学意义（t=2．417、2．444、2．633、2．579、2．525,均P〈0．05）。结论硫辛酸联合缬沙坦可有效治疗早期糖尿病肾病,下调其氧化应激水平,效果优于单独应用缬沙坦。     

Lipoic acid effects on renal function, aminopeptidase activities and oxidative stress in Crotalus durissus terrificus envenomation in mice

Crotalus durissus terrificus envenomation has been associated with direct nephrotoxicity, rhabdomyolysis, hyperuricemia, urinary hypoosmolality, alterations in aminopeptidase activities (AP) and oxidative stress. This study evaluated the effects of lipoic acid (LA) on renal function, lethality, AP and GSSG/GSH in mice injected with C. d. terrificus venom (vCdt). The doses and routes of administration of LA and vCdt promoted no systemic myotoxicity. LA did not alter significantly the lethality of vCdt. In nonenvenomed, LA induced hypercreatinemia, urinary hyperosmolality, decrease of urinary urea and creatinine, increase of protein in plasma and in soluble fraction (SF) and decrease in membrane-bound fraction (MF) of cortex and medulla. Decreased levels of all AP (except neutral-AP in MF-medulla) were also induced by LA in nonenvenomed. LA associated with vCdt decreased plasma osmolality, hematocrit, urinary uric acid, but increased urinary and SF-medullar protein. LA mitigated the increase of protein in SF-cortex and corrected hyperuricemia, GSSG/GSH and protein in MF-cortex and MF-medulla, as well as decreased plasma neutral AP and acid AP in MF-medulla of envenomed mice. Data suggest that LA contributes to the solubilization/remotion of proteins in MF with impairment of most AP, but it could be beneficial for the treatment of the direct nephrotoxicity of vCdt.     

Ursodeoxycholic acid does not affect ethinylestradiol bioavailability in women taking oral contraceptives

Objective Contraception is recommended for female patients during ursodeoxycholic acid (UDCA) treatment for the potential teratogenic effect of this bile acid, and the aim of our study was to determine whether this treatment affects the bioavailability of ethinylestradiol (EE₂).Methods In this double-blind, randomised study, we measured EE₂ pharmacokinetics in eight healthy volunteers randomly allocated to receive oral contraceptive (30 g EE₂ and 75 g gestodene) plus either UDCA (8–10 mg/kg per day) or placebo for 21 days during the first of three consecutive menstrual cycles. After a washout period during the second cycle, the subjects received the alternative treatment during the third menstrual cycle. Serum EE₂ and UDCA were measured using radioimmunoassay and gas chromatography–mass spectrometry, respectively. Results The profile for serum EE₂ concentration was similar during UDCA (mean maximum serum concentration 177 pg/ml, SEM 59) and during placebo treatment (153 pg/ml, SEM 62), and mean area under the curve (AUC) was 1374 pg/h per ml (SEM 580) and 1320 pg/h per ml (SEM 551) during the two regimens, respectively. The point estimates and 90% confidence intervals of UDCA/placebo ratios for EE₂ AUC and for maximum serum concentration were 1.1 (0.8–1.5) and 1.2 (1.0–1.4), respectively. Mean serum triglycerides concentration increased from 58.3 mg/dl (SEM 6.8) at enrolment to 91.4 mg/dl (SEM 10.7) during placebo (P<0.01) and to 88.6 mg/dl (SEM 13.7) during UDCA treatment (P<0.05). During UDCA treatment, serum enrichment with this bile acid and with the metabolite iso-UDCA was 29% (16%) and 3% (2%), respectively.Conclusion Co-administration with UDCA does not affect the bioavailability of EE₂ in healthy volunteers, indicating that contraceptive efficacy is not affected.     

Alpha-lipoic acid protects oxidative stress,changes in cholinergic system and tissue histopathology during co-exposure to arsenic-dichlorvos in rats

We investigated protective efficacy of α-lipoic acid (LA), an antioxidant against arsenic and DDVP co-exposed rats. Biochemical variables suggestive of oxidative stress, neurological dysfunction, and tissue histopathological alterations were determined. Male rats were exposed either to 50 ppm sodium arsenite in drinking water or in combination with DDVP (4 mg/kg, subcutaneously) for 10 weeks. α-Lipoic acid (50 mg/kg, pos) was also co-administered in above groups. Arsenic exposure led to significant oxidative stress along, hepatotoxicity, hematotoxicity and altered brain biogenic amines levels accompanied by increased arsenic accumulation in blood and tissues. These altered biochemical variables were supported by histopathological examinations leading to oxidative stress and cell death. These biochemical alterations were significantly restored by co-administration of α-lipoic acid with arsenic and DDVP alone and concomitantly. The results indicate that arsenic and DDVP induced oxidative stress and cholinergic dysfunction can be significantly protected by the supplementation of α-lipoic acid.     

Acute iron overload and oxidative stress in brain

An in vivo model in rat was developed by intraperitoneally administration of Fe-dextran to study oxidative stress triggered by Fe-overload in rat brain. Total Fe levels, as well as the labile iron pool (LIP) concentration, in brain from rats subjected to Fe-overload were markedly increased over control values, 6 h after Fe administration. In this in vivo Fe overload model, the ascorbyl (A)/ascorbate (AH^?) ratio, taken as oxidative stress index, was assessed. The A/AH^? ratio in brain was significantly higher in Fe-dextran group, in relation to values in control rats. Brain lipid peroxidation indexes, thiobarbituric acid reactive substances (TBARS) generation rate and lipid radical (LR) content detected by Electron Paramagnetic Resonance (EPR), in Fe-dextran supplemented rats were similar to control values. However, values of nuclear factor-kappaB deoxyribonucleic acid (NFκB DNA) binding activity were significantly increased (30%) after 8 h of Fe administration, and catalase (CAT) activity was significantly enhanced (62%) 21 h after Fe administration. Significant enhancements in Fe content in cortex (2.4 fold), hippocampus (1.6 fold) and striatum (2.9 fold), were found at 6 h after Fe administration. CAT activity was significantly increased after 8 h of Fe administration in cortex, hippocampus and striatum (1.4 fold, 86, and 47%, respectively). Fe response in the whole brain seems to lead to enhanced NF-κB DNA binding activity, which may contribute to limit oxygen reactive species-dependent damage by effects on the antioxidant enzyme CAT activity. Moreover, data shown here clearly indicate that even though Fe increased in several isolated brain areas, this parameter was more drastically enhanced in striatum than in cortex and hippocampus. However, comparison among the net increase in LR generation rate, in different brain areas, showed enhancements in cortex lipid peroxidation, without changes in striatum and hippocampus LR generation rate after 6 h of Fe overload. This information has potential clinical relevance, as it could be the key to understand specific brain damage occurring in conditions of Fe overload.     

Flosequinan does not affect systemic and regional vascular responses to simulated orthostatic stress in healthy volunteers.

1. The effects of a single oral dose (100 mg) of flosequinan on systemic and regional (forearm, splanchnic and renal) vascular responses to simulated orthostatic stress (lower body negative pressure, LBNP) were investigated in nine healthy male volunteers, in a double-blind, placebo-controlled crossover study. 2. Forty-five minutes after its administration and before LBNP, flosequinan induced a significant decrease in total peripheral and in forearm vascular resistances without any concomitant change in arterial pressure, in heart rate and in the investigated biological parameters (plasma catecholamines, arginine vasopressin and renin activity). 3. After flosequinan and placebo, LBNP induced similar decreases in central venous pressure at all levels of LBNP (-10, -20 and -40 mm Hg) and in pulse pressure at LBNP -40 mm Hg. LBNP-induced increase in forearm vascular resistance was significantly more marked after flosequinan than after placebo at all levels of LBNP, and this was also true for splanchnic vascular resistance but at LBNP -40 mm Hg only. However, inasmuch as the basal values of these two parameters before LBNP were lower after flosequinan than after placebo, their final values after LBNP -40 mm Hg were similar. Finally, LBNP-induced changes in renal vascular resistance, glomerular filtration rate and filtration fraction as well as in plasma catecholamines, arginine vasopressin and renin activity were similar after flosequinan and placebo at all levels of LBNP. 4. Flosequinan affected neither reflex control of heart rate (phenylephrine test) nor non-specific vasoconstrictor responses (cold pressor test). (ABSTRACT TRUNCATED AT 250 WORDS)     

Low single dose gabapentin does not affect prefrontal and occipital gamma-aminobutyric acid concentrations

The γ-aminobutyric acid (GABA) system has been proposed as a target for novel antidepressant and anxiolytic treatments. Emerging evidence suggests that gabapentin (GBP), an anticonvulsant drug that significantly increases brain GABA levels, is effective in the treatment of anxiety disorders. The current study was designed to measure prefrontal and occipital GABA levels in medication-free healthy subjects after taking 0 mg, 150 mg and 300 mg GBP. Subjects were scanned on a 3T scanner using a transmit-receive head coil that provided a relatively homogenous radiofrequency field to obtain spectroscopy measurement in the medial prefrontal (MPFC) and occipital cortex (OCC). There was no dose-dependent effect of GBP on GABA levels in the OCC or MPFC. There was also no effect on Glx, choline or N-acetyl-aspartate concentrations. The previously reported finding of increased GABA levels after GBP treatment is not evident for healthy subjects at the dose of 150 and 300 mg. As a result, if subjects are scanned on a 3T scanner, low dose GPB is not useful as an experimental challenge agent on the GABA system.     

The potent calcitonin gene-related peptide receptor antagonist, telcagepant, does not affect nitroglycerin-induced vasodilation in healthy men

AIMS

To assess the effect of the calcitonin gene-related peptide (CGRP) receptor antagonist, telcagepant, on the haemodynamic response to sublingual nitroglycerin (NTG).

METHODS

Twenty-two healthy male volunteers participated in a randomized, placebo-controlled, double-blind, two-period, crossover study. Subjects received 500 mg telcagepant or placebo followed, 1.5 h later, by 0.4 mg NTG. To assess the haemodynamic response the following vascular parameters were measured: blood pressure, aortic augmentation index (AIx) and brachial artery diameter (BAD). Data are presented as mean (95% confidence interval, CI).

RESULTS

The aortic AIx following NTG decreased by −18.50 (−21.02, −15.98) % after telcagepant vs. −17.28 (−19.80, −14.76) % after placebo. The BAD fold increase following NTG was 1.14 (1.12, 1.17) after telcagepant vs. 1.13 (1.10, 1.15) after placebo. For both AIx and BAD, the hypothesis that telcagepant does not significantly affect the changes induced by NTG is supported (P < 0.0001). In addition, no vasoconstrictor effect of telcagepant could be demonstrated.

CONCLUSIONS

Telcagepant did not affect NTG-induced haemodynamic changes. These data suggest that NTG-induced vasodilation is not CGRP dependent.     

Low doses of recombinant human erythropoietin does not affect C‐terminal FGF23 in healthy men

Recombinant human erythropoietin (rhEpo) can improve human performance, but misuse remains difficult to detect. C‐terminal fibroblast growth factor 23 (cFGF23) was recently demonstrated to increase following injection of a single high dose rhEpo, but the effect of more frequent low doses is unknown. Using a randomized double‐blind placebo‐controlled design, we investigated whether 2 weeks of subcutaneous injections three times a week of 50 IU/kg Eprex (low‐dose) or 20 IU/kg Eprex (micro‐dose) increase cFGF23 levels compared with saline (placebo) injections in 24 healthy males. Venous blood was sampled at day ?3, 0, 1, 3, 11, 14, 18, and 25 of the treatment and analyzed for cFGF23 and erythropoietin concentration ([EPO]). The level of cFGF23 was similar at days ?3, 0, 1, 3, 11, 14, 18, and 25 with the low‐dose (23 ± 4, 26 ± 5, 23 ± 7, 27 ± 6, 25 ± 8, 24 ± 10, 22 ± 5, and 24 ± 7 RU/mL, respectively), micro‐dose (23 ± 6, 25 ± 5, 23 ± 8, 28 ± 9, 27 ± 7, 25 ± 9, 25 ± 5, and 23 ± 6 RU/mL, respectively) and placebo (23 ± 6, 24 ± 6, 26 ± 7, 26 ± 6, 31 ± 6, 31 ± 7, 24 ± 4, and 27 ± 8 RU/mL, respectively) treatment. The correlation coefficient between plasma [EPO] and plasma cFGF23 levels was R² = 0.01 and insignificant. The results demonstrate that cFGF23 is not sensitive to low doses of subcutaneous rhEpo injections in healthy males.     

Pharmacokinetics of lipoic acid in healthy Chinese volunteers after single and multiple doses of Lipoic acid dispersible tablets

This study aimedto evaluate the pharmacokinetics for lipoic acid (LA) after oral administration of 12 healthy Chinese volunteers with single and multiple-dose of lipoic acid dispersal tablets using a liquid chromatography-temdend mass spectrometry (LC-MS/MS) methods. In single-dose study, healthy Chinese male and female volunteers received three dose levels at 0.2, 0.3, and 0.4 g of LA dispersal tablets with a 3×3 Latina square design. In multiple-dose study, 12 healthy Chinese volunteers received orally a 0.1 g of LA dispersible tablet three times daily for 6 consecutive days and 0.3 g once on day 7. The results showed that pharmacokinetics of LA fitted a two-compartment open model. The values of area under the curve (AUC) increased proportionally within the range of 0.2–0.4 g, while the Vd/F, CL/F, MRT, t_1/2 and t_max of LA were similar at three dose levels. The steady-state pharmacokinetic parameters of LA were similar to those following a single dose and no accumulation was found following multiple-dose of LA dispersal tablets.     

硫辛酸对早期糖尿病肾病患者体内氧化应激、炎性反应的调节及足细胞的保护作用

目的 观察硫辛酸对早期糖尿病肾病(DKD)患者体内氧化应激、炎性反应的调节作用及足细胞的保护作用.方法 选择2016年1月-2017年12月就诊于安徽省太湖县人民医院内一科的早期DKD患者60例,采用随机数字表法分为治疗组和对照组各30例.治疗组给予硫辛酸注射液静脉滴注,对照组给予0.9％氯化钠注射液静脉滴注.比较2组...     

Serotonin depletion by 5,7-dihydroxytryptamine or para-chloroamphetamine does not affect cancer anorexia

Anorectic tumor-bearing rats exhibited increased brain levels of the 5-HT precursor, tryptophan, and metabolite, 5-hydroxindoleactic acid (5-HIAA). In an effort to determine whether indoleamine systems had any role in the etiology of cancer anorexia the anorectic effects of cancer (Walker 256 carcinosarcoma) were investigated in immature female rats that had been depleted of brain serotonin (5-HT) by the intracisternal injection of 5,7-dihydroxytryptamine (5,7-DHT) or the systemic injection of para-chloroamphetamine (PCA). Although both 5,7-DHT and PCA significantly reduced brain concentrations of 5-HT and 5-HIAA by approximately 50%, no effects on the onset or severity of the anorectic response to cancer were observed. Similarly, neither drug affected eating in non-tumor-bearing control animals. Therefore, these data do not support increased brain 5-HT activity as a primary mediator of cancer anorexia.     

The influence of oxidative stress on various inotropic responses in isolated rat left atria

The effects of free radicals, generated by electrolysis of a physiological salt solution, on various inotropic responses to drugs in isolated rat left atria were studied. Evidence for the generation of hydroxyl radicals was obtained from an appropriate fluorimetric assay. The amount of free radicals produced by electrolysis of the medium proved current-dependent. Exposure of isolated rat left atria to the medium which had been subjected to electrolysis caused a current-dependent decrease in contractile force. Oxidative stress, as a result of the electrolysis of the medium, caused altered inotropic responses to extra cellular Ca²⁺ (pD₂ control group: 2.62 ± 0.06 vs. 2.44 ± 0.07 electrolysis group), sodium withdrawal (rise in contractile force control group: 1.73 ± 0.19 mN vs. 0.48 ± 0.21 mN electrolysis group) and lowering of stimulation frequency. The response to isoprenaline was diminished in atria subjected to oxidative stress and led to a rightward shift of the concentration response curves (pD₂ control group: 7.56 ± 0.10 vs. 6.77 ± 0.11 electrolysis group). In addition, the inotropic responses to forskolin (pD₂ control group: 6.17 ± 0.12 vs. < 4.5 electrolysis group) and dibutyryl cAMP (rise in contractile force caused by 1 × 10^–5 M db-cAMP in control group: 2.15 ± 0.01 mN vs. 1.21 ± 0.10 mN electrolysis group) proved blunted as well. Measurement of the adenylyl cyclase activity revealed that free radicals attenuated the basal (by 11.1%) and forskolin stimulated (155.0 ± 5.1 vs. 48.0 ± 1.8 pmol cAMP/mg prot./min for control and electrolysis group respectively) activity of the adenylyl cyclase. DMSO, a well known hydroxyl radical scavenger, was able to abolish the free radical-induced decrease in the response to isoprenaline. Surprisingly, addition of α-adrenoceptor agonists to atria subjected to electrolysis-generated free radicals led to a rapid decrease in contractile force. DMSO was unable to counteract the negative intropic effect of methoxamine in atria subjected to oxidative stress. This negative inotropic response to α-adrenoceptor agonists in atria subjected to electrolysed medium is unlikely to be the direct result of phospholipase C or protein kinase C activation. Angiotensin II (which stimulates PLC as well) did not reduce contractile force and chelerythrine (a PKC inhibitor) was unable to counteract the negative inotropic effect of the adrenoceptor agonists. In addition, the negative inotropic effect of methoxamine proved insensitive to 10^–6 M phentolamine and 10^–5 M doxazosin, which indicates an α-adrenoceptor independent mechanism. From this study we conclude that free radicals alter responses to various inotropic stimuli. These alterations may be the result of injured contractile elements, transporter molecules and molecules involved in signal transduction. Addition of α-adrenoceptor agonists after oxidative stress leads to a α-adrenoceptor, PLC and PKC independent decrease in contractile force. Received: 17 June 1996 / Accepted: 6 November 1996     

Cicletanine does not affect plasma atrial natriuretic peptide concentration in healthy subjects

Summary The effect of 50 and 150 mg cicletanine, a new vasodilator antihypertensive, on plasma atrial natriuretic peptide (ANP), cyclic GMP and antidiuretic hormone has been investigated at rest and during standardized exercise, in a double blind cross over study in healthy subjects.Exercise significantly increased the plasma ANP, cyclic GMP and antidiuretic hormone concentrations, and cicletanine did not affect any of them either at rest or during exercise.Since the alpha-1 adrenoceptor blocker prazosine decreases, beta-adrenoceptor blockers increase and the vasodilator cicletanine does not alter the plasma ANP response to exercise, it is suggested that adrenergic receptors may be directly involved in the regulation of ANP secretion.     

Expression and antioxidant function of liver fatty acid binding protein in normal and bile-duct ligated rats

Liver fatty acid binding protein has recently been shown to possess antioxidant properties but its role in liver disease, such as cholestasis, is not known. Since oxidative stress has been recognized as an important contributing factor in liver disease, we investigated the expression and antioxidative function of this protein using the bile-duct ligated model of cholestasis. Rats were divided into 3 groups: sham, bile-duct ligated and bile-duct ligated plus clofibrate. Animals were sacrificed at various time points after bile-duct ligation. RT-PCR and Western blot were used to analyze liver fatty acid binding protein expression. Cellular lipid peroxidation products were assessed by measuring thiobarbituric acid-reactive substances. Liver function was evaluated by measuring serum total bilirubin, alanine aminotransferase and ammonia. Liver fatty acid binding protein mRNA and protein levels were reduced to 51% and 20% of sham, respectively at 2 weeks following bile-duct ligation (p<0.05). The decreased liver fatty acid binding protein was associated with a statistical increase in hepatic lipid peroxidation products (224%) and decrease in hepatic function. Clofibrate treatment restored protein level and improved hepatic function. Clofibrate treatment also reduced hepatic lipid peroxidation products by 68% as compared with the bile-duct ligated group (p<0.05). Liver fatty acid binding protein likely has important antioxidant function during hepatocellular oxidative stress.     

Effects of acute alcohol consumption and vitamin E co-treatment on oxidative stress parameters in rats tongue

The aim of this study was to evaluate the effects of acute alcohol consumption and vitamin E co-treatment upon oxidative stress parameters in rats tongue. Thirty-eight, Wistar rats were separated into five groups (alcohol, alcohol/vitamin E, control, Tween, vitamin E). Alcohol and alcohol vitamin E groups had the standard diet, and 40% alcohol on drinking water. Other groups were fed with the same standard diet and water ad libitum. Vitamin E was given by gavage to vitamin E and alcohol/vitamin E rats twice a week. Alcohol and control groups were subjected to saline gavage and Tween group to 5% Tween 80 solution, the vitamin E vehicle. At day 14, the animals were anesthetized and specimens were obtained from tongue. Lipid peroxidation (TBARS), protein oxidative damage, catalase (CAT) and superoxide dismutase (SOD) activities were quantified. Alcohol group decreased TBARS in relation to control group and alcohol vitamin-treated animals decreased TBARS when compared to Tween and vitamin E groups. SOD activity was lower and CAT activity was higher in animals treated with both alcohol and vitamin E. These results suggest that short-term alcohol consumption decreases lipid peroxidation levels. Alternatively, alcohol/vitamin E group increased CAT, showing the toxicity of this association.