Effect of betaine supplementation on plasma nitrate/nitrite in exercise-trained men

Background: Betaine, beetroot juice, and supplemental nitrate have recently been reported to improve certain aspects of exercise performance, which may be mechanistically linked to increased nitric oxide. The purpose of the present study was to investigate the effect of betaine supplementation on plasma nitrate/nitrite, a surrogate marker or nitric oxide, in exercise-trained men.Methods: We used three different study designs (acute intake of betaine at 1.25 and 5.00 grams, chronic intake of betaine at 2.5 grams per day for 14 days, and chronic [6 grams of betaine per day for 7 days] followed by acute intake [6 grams]), all involving exercise-trained men, to investigate the effects of orally ingested betaine on plasma nitrate/nitrite. Blood samples were collected before and at 30, 60, 90, and 120 min after ingestion of 1.25 and 5.00 grams of betaine (Study 1); before and after 14 days of betaine supplementation at a dosage of 2.5 grams (Study 2); and before and after 7 days of betaine supplementation at a dosage of 6 grams, followed by acute ingestion of 6 grams and blood measures at 30 and 60 min post ingestion (Study 3).Results: In Study 1, nitrate/nitrite was relatively unaffected and no statistically significant interaction (p = 0.99), dosage (p = 0.69), or time (p = 0.91) effects were noted. Similar findings were noted in Study 2, with no statistically significant interaction (p = 0.57), condition (p = 0.98), or pre/post intervention (p = 0.17) effects noted for nitrate/nitrite. In Study 3, no statistically significant changes were noted in nitrate/nitrite between collection times (p = 0.97).Conclusion: Our data indicate that acute or chronic ingestion of betaine by healthy, exercise-trained men does not impact plasma nitrate/nitrite. These findings suggest that other mechanisms aside from increasing circulating nitric oxide are likely responsible for any performance enhancing effect of betaine supplementation. © 2011 Bloomer et al; licensee BioMed Central Ltd

Effects of betaine on lipopolysaccharide-induced memory impairment in mice and the involvement of GABA transporter 2

<p>Abstract</p> <p>Background</p> <p>Betaine (glycine betaine or trimethylglycine) plays important roles as an osmolyte and a methyl donor in animals. While betaine is reported to suppress expression of proinflammatory molecules and reduce oxidative stress in aged rat kidney, the effects of betaine on the central nervous system are not well known. In this study, we investigated the effects of betaine on lipopolysaccharide (LPS)-induced memory impairment and on mRNA expression levels of proinflammatory molecules, glial markers, and GABA transporter 2 (GAT2), a betaine/GABA transporter.</p> <p>Methods</p> <p>Mice were continuously treated with betaine for 13 days starting 1 day before they were injected with LPS, or received subacute or acute administration of betaine shortly before or after LPS injection. Then, their memory function was evaluated using Y-maze and novel object recognition tests 7 and 10-12 days after LPS injection (30 μg/mouse, i.c.v.), respectively. In addition, mRNA expression levels in hippocampus were measured by real-time RT-PCR at different time points.</p> <p>Results</p> <p>Repeated administration of betaine (0.163 mmol/kg, s.c.) prevented LPS-induced memory impairment. GAT2 mRNA levels were significantly increased in hippocampus 24 hr after LPS injection, and administration of betaine blocked this increase. However, betaine did not affect LPS-induced increases in levels of mRNA related to inflammatory responses. Both subacute administration (1 hr before, and 1 and 24 hr after LPS injection) and acute administration (1 hr after LPS injection) of betaine also prevented LPS-induced memory impairment in the Y-maze test.</p> <p>Conclusions</p> <p>These data suggest that betaine has protective effects against LPS-induced memory impairment and that prevention of LPS-induced changes in GAT2 mRNA expression is crucial to this ameliorating effect.</p

Protective effect of leptin against ischemia-reperfusion injury in the rat small intestine

BACKGROUND: The small intestine is extremely sensitive to ischemia-reperfusion (I/R) injury and a range of microcirculatory disturbances which contribute to tissue damage. Previous studies have shown that leptin plays an important physiological role in the microvasculature. The aim of this study was to evaluate the protective effects of leptin in I/R – induced mucosal injury in the small intestine. METHODS: Forty rats were divided into 5 groups (n = 8). Group I was subjected to a sham operation. Following mesenteric ischemia in group II (control); physiologic saline 1 cm(3), in group III; leptin 100 μg/kg, and physiologic saline 1 cm(3), in group IV; N(G)-L-arginine methyl ester (L-NAME) 20 mg/kg, and physiologic saline 1 cm(3), in group V; leptin 100 μg/kg, L-NAME 20 mg/kg, and physiologic saline 1 cm(3 )were given intra-peritoneally. In these groups, an I/R procedure was performed by occlusion of the superior mesenteric artery for 45 min followed by 120 min reperfusion. After reperfusion, the small intestines were resected for malondialdehyde (MDA) and nitric oxide (NO) concentration and histopathologic properties. Mucosal lesions were scored between 0 and 5. Tissue MDA and NO concentration and histopathologic grades were compared statistically. RESULTS: Tissue MDA level significantly increased (P < 0.05), tissue NO level significantly decreased in group V animals, compared to group III animals respectively (P < 0.001). Histopathologically, intestinal injury significantly decreased in the leptin treated ischemic group. CONCLUSION: Leptin can be used safely in mesenteric occlusive diseases, since it induces NO formation and release in mesenteric vessels

Post-Operative Pain After Knee Arthroscopy and Related Factors

The aim of this study was to explore the intensity of post-arthroscopy knee pain during the first 24 hours, and to study the influence of pre-operative pain, tourniquet time and amount of surgical trauma on post-arthroscopy pain. In 78 male patients that underwent elective arthroscopic menisectomy or diagnostic arthroscopy of the knee, preoperative and post-operative pain were registered using the Visual Analogue Scale. Variance for repeated measures and for independent observations was analysed. Supplementary analgesia was required for 23% of the patients, more often in the recovery room and between 2 and 8 hours postoperatively. Of all factors analyzed, only time was statistically significant in determining the level of post-operative pain. Supplementary analgesia was required only in patients that underwent operative arthroscopy, and more often in patients with tourniquet time of more than 40 minutes. In conclusions, post-operative time is the most significant factor related to the post-arthroscopy knee pain

Lack Of Effect Of N-Acetylcysteine Treatment To Ameliorate The Progression Of Multiple Organ Failure

Objective: To investigate whether prolonged infusion of the oxygen free radical scavenger N-acetylcysteine (NAC) that is commenced immediately after admission to intensive care unit (ICU) could ameliorate the development or progression of multiple organ failure (MOF). Methods: After receiving ethical committee approval, a prospective randomized, double-blind, placebo controlled study was performed in the Anesthesiology and Reanimation Intensive Care Unit, Hacettepe University Hospital, Ankara, Turkey between December 2002 and May 2003. Twenty-six patients were randomized to receive either NAC in 5% dextrose 40 mg/kg/day or the same volume of 5% dextrose both in 4 divided doses. Two patients were withdrawn due to ICU stay <24 hours. Treatment effect on organ function was assessed by the sequential organ failure assessment (SOFA) scores according to physiological parameters of respiratory, hematological, hepatic, cardiovascular, central nervous system (CNS) and renal system scores that were obtained on admission, then daily. Chi-square, Mann Whitney U tests were used for statistical analysis. Results: There was no significant difference between the 2 groups in any of the 5 organ dysfunction parameters, total maximum SOFA, delta SOFA length of intensive care stay, days of mechanical ventilation and mortality. In the NAC treatment group, the maximum SOFA coagulation score was higher than the control group (p<0.05). Conclusion: N-acetylcysteine (40 mg/kg/day) that was commenced immediately after admission to ICU did not ameliorate the progression of MOF in this small cohort of patients. We believe routine prophylactic use of low-dose NAC in all critically ill patients does not provide positive protection.Wo

alcohol consumption: Pseudomonas aeruginosa induced pneumonia rat model

In this study, our aim was to investigate whether cellular alterations occurred in liver and lung tissue in presence of chronic alcohol ingestion and Pseudomonas aeruginosa pneumonia related to oxidative stress and in situ cell death. Male wistar rats were divided into five groups: the sham group fed by normal solid diet, two control groups; one fed by normal liquid diet, and the other fed by liquid diet plus ethanol, two pneumonia groups induced by Pseudomonas aeruginosa; one fed by normal liquid diet, and the other fed by liquid diet plus ethanol. Terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labelling analysis was performed to confirm in situ cell death. Serum alanine amino transferase and lactate dehydrogenase activities, and tissue and serum malondialdehyde levels, paraoxonase, arylesterase activities, and tissue caspase-3 activities were determined. Serum alanine amino transferase activities of both ethanol given groups were higher than the other groups (p<0.05). Liver malondialdehyde level was increased in ethanol with pneumonia group (p<0.05). Lung malondialdehyde levels were not different among groups. Terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labelling positive cell ratio in the liver was higher in both ethanol given groups and normal liquid diet with pneumonia group than sham and control group fed by normal liquid diet. Liver and lung caspase-3 activities were not different among groups. Although serum paraoxonase activities were lower in both pneumonia groups, it was not statistically significant. It may be interpreted as growing infection during chronic ethanol ingestion that causes increased liver damage through oxidative stress

alcohol consumption: Pseudomonas aeruginosa induced pneumonia rat model

In this study, our aim was to investigate whether cellular alterations occurred in liver and lung tissue in presence of chronic alcohol ingestion and Pseudomonas aeruginosa pneumonia related to oxidative stress and in situ cell death. Male wistar rats were divided into five groups: the sham group fed by normal solid diet, two control groups; one fed by normal liquid diet, and the other fed by liquid diet plus ethanol, two pneumonia groups induced by Pseudomonas aeruginosa; one fed by normal liquid diet, and the other fed by liquid diet plus ethanol. Terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labelling analysis was performed to confirm in situ cell death. Serum alanine amino transferase and lactate dehydrogenase activities, and tissue and serum malondialdehyde levels, paraoxonase, arylesterase activities, and tissue caspase-3 activities were determined. Serum alanine amino transferase activities of both ethanol given groups were higher than the other groups (p<0.05). Liver malondialdehyde level was increased in ethanol with pneumonia group (p<0.05). Lung malondialdehyde levels were not different among groups. Terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labelling positive cell ratio in the liver was higher in both ethanol given groups and normal liquid diet with pneumonia group than sham and control group fed by normal liquid diet. Liver and lung caspase-3 activities were not different among groups. Although serum paraoxonase activities were lower in both pneumonia groups, it was not statistically significant. It may be interpreted as growing infection during chronic ethanol ingestion that causes increased liver damage through oxidative stress

Comparison Of Halothane, Enflurane And Isoflurane Kidney Effects Through Alanine Aminopeptidase Urine Creatinine Values

The kidney effects of halothane, enflurane and isoflurane were evaluated by using the ratio of urinary excretion of alanine aminopeptidase (AAP) to urine creatinine. Thirty patients in ASA class 1 or 2 were studied, None had renal disease nor received nephrotoxic drugs. Groups 1, 2 and 3 received halothane, enflurane and isoflurane respectively, Creatinine and AAP activities in urine spot tests, serum creatinine and BUN levels were determined preoperatively and on the first and second postoperative days. Urine AAP activity and AAP/urine creatinine values increased significantly on the first and second postoperative days compared with the preoperative values in all groups (P < 0.05). The present study did not reveal any significant difference in the kidney effects of halothane, enflurane and isoflurane through AAP/creatinine in spot urine values.Wo