Phase angle is related to oxidative stress and antioxidant biomarkers in breast cancer patients undergoing chemotherapy.

PURPOSE: The study aimed to analyze the influence of chemotherapy on health biomarkers and examine the relationship between phase angle (PhA) and oxidative stress. METHODS: A prospective study was performed. Women who were starting chemotherapy were recruited. Also, this study included a control group of women without cancer. Bioelectrical impedance multiple-frequency (BIS) analysis, 24h food recall, and blood samples were collected at 2-time points: diagnosis (T0) and after one month of completion of therapy (T1) for the main study group and one-time point for the control group. T-tests or Mann-Whitney Wilcoxon Test was used to compare variables. Linear regression analysis was conducted to test if PhA is related to the dependent variables after adjusting for age and body mass index. RESULTS: 119 women were included (61 with breast cancer and 58 healthy). There was no difference between the groups concerning anthropometrics, fat mass, and fat-free mass. Breast cancer patients had a worsening in PhA (p<0.001) after chemotherapy completion. PhA was positive statistically correlated with extracellular water, albumin, and the antioxidant markers at both times. The linear model showed that PhA was significantly predicted by C reactive protein, 2,2-Diphenyl-1-picrylhydrazyl (DPPH), Malondialdehyde (MDA), total body water/extracellular water, and body mass index fat mass. This model explained 58% of PhA variability (p<0.001). CONCLUSION: Our findings show that PhA is an easy and affordable tool that correlates oxidative stress markers in breast cancer patients, regardless of age or body mass index.

Phase angle and cellular health: inflammation and oxidative damage.

Phase angle is a composite measure that combines two raw bioelectrical impedance analysis measures: resistance and reactance. Phase angle has been considered an indicator of cellular health, integrity, and hydration. As inflammation and oxidative stress can damage cellular structures, phase angle has potential utility in early detecting inflammatory and oxidative status. Herein, we aimed to critically review the current understanding on the determinants of phase angle and its relationship with markers of inflammation and oxidative stress. We also discussed the potential role of phase angle in detecting chronic inflammation and related adverse outcomes. Several factors have been identified as predictors of phase angle, including age, sex, extracellular to intracellular water ratio, and fat-free mass. In addition to these factors, body mass index (BMI) also seems to influence phase angle. Available data also show that lower phase angle values are correlated (negligible to high correlation coefficients) with higher c-reactive protein, tumour necrosis factor-α, interleukin-6, and interleukin-10 in studies involving the general and aging populations, as well as patients with chronic conditions. Although fewer studies have evaluated the relationship between phase angle and markers of oxidative stress, available data also suggest that phase angle has potential to be used as an indicator (for screening) of oxidative damage. Future studies including diverse populations and bioelectrical impedance devices are required to confirm the validity and accuracy of phase angle as a marker of inflammation and oxidative stress for clinical use.

An Evaluation of Metabolic, Dietetic, and Nutritional Status Reveals Impaired Nutritional Outcomes in Breast Cancer Patients.

Nutritional status can change in breast cancer patients after treatment. However, the metabolic implications of those alterations are poorly understood. We used a cross-sectional study design to compare body composition, lipids, glucose levels, and adiposity indices in breast cancer patients with a matched control and a healthy group. We recruited women who completed their chemotherapy (BC group) and compared them with a group of women without cancer age and body mass index-paired (MC group) and a group of healthy women (HC group). We estimated body composition by bioelectrical impedance analysis, physical function by handgrip strength, and food consumption by 24-hour food record. A blood sample was collected. We calculated visceral obesity indices (VAI and LAP) and insulin resistance-triglyceride glucose (TyG). Eighty-eight women were included (BC = 36, MC = 36, HC = 16). BC patients demonstrated worse phase angle values, nutritional risk index and lower handgrip strength. Additionally, according to the indices, BC had impairments in lipids, worse glucose levels, and elevated visceral fat adiposity and presented important unhealthy dietary patterns characterized by under-recommended protein consumption and higher caloric intake than the other groups. No differences were observed between both control groups. Further investigations are required to examine the underlying mechanisms and the potential longitudinal changes during surveillance.

Effect of chocolate on older patients with cancer in palliative care: a randomised controlled study.

BACKGROUND: Older advanced stage cancer patients, with changes in nutritional status, represent an important demand for palliative care. The aim was to determine the effects of 4 weeks of chocolate consumption on the nutritional status of older cancer patients in palliative care. METHODS: Older cancer patients in palliative care with ambulatory (n = 46) monitoring were randomized to control (CG, n = 15), intervention with 55% cocoa chocolate (IG1, n = 16) and intervention with white chocolate (IG2, n = 15) groups and evaluated before and after 4 weeks for nutritional status (primary outcome), evaluated by the Mini Nutritional Assessment tool (MNA). Food consumption, anthropometry, body composition, laboratory parameters and quality of life (QL) with the European Organization for the Research and Treatment of Cancer instrument were also evaluated. RESULTS: IG1 progressed with increased screening (estimated difference [95% CI]: - 1.3 [- 2.2;-0.4], p < 0.01), and nutritional (estimated difference [95% CI]: - 1.3 [- 2.5;-0.1], p = 0.04) scores on the MNA, with no change in anthropometry and body composition. Regarding antioxidant capacity, reduced glutathione levels increased (estimated difference [95% CI]: - 0.8 [- 1.6;-0.02], p = 0.04) and malondealdehyde levels decreased in IG2 (estimated difference [95% CI]:+ 4.9 [+ 0.7;+ 9.1], p = 0.02). Regarding QL, functionality improved in IG1, with higher score in the functional domain (estimated difference [95% CI]:-7.0 [- 13.3;-0.7], p = 0.03). CONCLUSIONS: The consumption of chocolate with a greater cocoa content may contribute to the improvement of the nutritional status and functionality among older cancer patients in palliative care. The consumption of white chocolate was associated with improved oxidative stress. TRIAL REGISTRATION: A randomized clinical trial (ClinicalTrials.gov NCT04367493 ).

Metabolic syndrome and unfavorable outcomes on body composition and in visceral adiposities indexes among early breast cancer women post-chemotherapy.

PURPOSE: The study objected to investigate potential changes in metabolic, dietary, and nutritional status in women with stages I-III breast cancer exposed to chemotherapy. METHODS: Women who were starting chemotherapy with no previous treatment were recruited. Anthropometrics, bioelectrical impedance analysis, handgrip strength, blood pressure and blood sample were collected. Visceral adiposity index and lipid accumulation product were calculated. Dietary intake was evaluated, and the multiple source methods program was applied. Metabolic syndrome (MetS) was assessed following the NCEP-ATP III criteria (defined as 3 of 5 components of MetS). All data were collected at 2-time points: diagnosis (T0) and after 1 month of completion of therapy (T1). Mean, standard deviation, percentage, and ANOVA in SAS Studio® were used to explore the results. RESULTS: 61 women were included. We did not find any changes in anthropometrics and body composition. However, phase angle, extracellular water (EX) and ratio EX to total body water had expressive changes (p < 0.001). The results showed changes in lipid profile (p < 0.001), and greater unfavorable outcomes on adiposities index (p < 0.001). At the end of the study, 68,8% (N = 42) of the women developed MetS post-chemotherapy. CONCLUSION: We have found supporting evidence for chemotherapy treatment resulting in worsening of nutritional markers, lipid profile and adiposity markers. After chemotherapy part of the sample developed MetS, even without changes in body weight, fat mass, and food intake. Breast cancer patients may benefit from targeted interventions before starting chemotherapy to prevent MetS post-treatment, and therefore reduce the risk of cardiovascular disease. Further investigation into this theme is needed.

Performance of functionality measures and phase angle in women exposed to chemotherapy for early breast cancer.

PURPOSE: The study aimed to analyze the influence of chemotherapy on nutritional status and the phase angle (PhA) as nutritional indicator for breast cancer women undergoing chemotherapy. METHODS: A prospective study was performed. Women who were starting chemotherapy with no previous chemotherapy treatment were recruited. Quality of life (QoL) was collected using the EORTC QLQ-BR23 questionnaire. Bioelectrical impedance analysis, performance tests, and blood sample to albumin analyzes were collected at 2-time points: diagnosis (T0) and after 1 month of completion of therapy (T1). Mean, standard deviation, linear regression, and ANOVA in R were used to explore the results. RESULTS: 61 women were included. We did not find any changes in body composition. However, PhA, nutritional risk index (NRI), gait speed (GS), and handgrip strength (HGS) had expressive changes (p < 0.001). 75.4% of women had PhA values below the cut-off point of 5.6°, and the group that had a lower average of PhA also expressed low NRI. PhA was a nutritional status marker and its values were influenced by changes in NRI (p < 0.05). CONCLUSION: We have found supporting evidence for chemotherapy treatment resulting in worsening of prognostic factors such as PhA, and yet PhA was related to no nutritional risk. Besides a higher prevalence of obesity, 80% of the sample showed some nutritional risk level, implying the possibility of a sub-notification candidate who might benefit, for instance, from nutritional intervention in obesity groups. Further investigation about this theme may improve health measures for the prevention and screening of disease among breast cancer.

Antioxidant Effect of Standardized Extract of Propolis (EPP-AF®) in Healthy Volunteers: A "Before and After" Clinical Study.

BACKGROUND: Propolis is rich in polyphenols, especially flavonoids and phenolic acids, and has significant antioxidant activity, shown mainly in "in vitro" studies. OBJECTIVE: The aim of this study was to evaluate the antioxidant efficacy and safety of a standardized propolis extract in healthy volunteers. DESIGN: A two-phase sequential, open-label, nonrandomized, before and after clinical trial. METHODS: Healthy participants received two EPP-AF® doses (375 and 750 mg/d, P.O, tid) during 7 ± 2 days, starting with the lower doses. Immediately before starting EPP-AF® administration and at the end of each 7-day dosing schedule, blood and urine samples were collected for quantification of 8-OHDG (8-hydroxydeoxyguanosine) and 8-ISO (8-isoprostanes) in urine and GSH (reduced glutathione), GSSG (oxidized glutathione), SOD (superoxide dismutase), FRAP (Ferric Reducing Antioxidant Power), vitamin E, and MDA (malondialdehyde) in plasma. RESULTS: In our study, we had 34 healthy participants (67.7% women, 30 ± 8 years old, 97% white). The 8-ISO, a biomarker of lipid peroxidation, decreased with both doses of EPP-AF® compared to baseline (8-ISO, 1.1 (0.9-1.3) versus 0.85 (0.75-0.95) and 0.89 (0.74-1.0), ng/mg creatinine, P < 0.05, for 375 and 750 mg/d EPP-AF® doses versus baseline, mean and CI 95%, respectively). 8-OHDG, a biomarker of DNA oxidation, was also reduced compared to baseline with 750 mg/d doses (8-OHDG, 15.7 (13.2-18.1) versus 11.6 (10.2-13.0), baseline versus 750 mg/d, respectively, ng/mg creatinine, P < 0.05). Reduction of biomarkers of oxidative stress damage was accompanied by increased plasma SOD activity (68.8 (66.1-73.3) versus 78.2 (72.2-80.5) and 77.7 (74.1-82.6), %inhibition, P < 0.0001, 375 and 750 mg/d versus baseline, median and interquartile range 25-75%, respectively) and by increased GSH for 375 mg/d EPP-AF® doses (1.23 (1.06-1.34) versus 1.33 (1.06-1.47), µmol/L, P < 0.05). CONCLUSION: EPP-AF® reduced biomarkers of oxidative stress cell damage in healthy humans, with increased antioxidant enzymatic capacity, especially of SOD. This trial is registered with the Brazilian Registry of Clinical Trials (ReBEC, RBR-9zmfs9).

Hepatic Osteodystrophy: The Mechanism of Bone Loss in Hepatocellular Disease and the Effects of Pamidronate Treatment.

OBJECTIVES:: The present study was designed to evaluate the bone phenotypes and mechanisms involved in bone disorders associated with hepatic osteodystrophy. Hepatocellular disease was induced by carbon tetrachloride (CCl4). In addition, the effects of disodium pamidronate on bone tissue were evaluated. METHODS:: The study included 4 groups of 15 mice: a) C = mice subjected to vehicle injections; b) C+P = mice subjected to vehicle and pamidronate injections; c) CCl4+V = mice subjected to CCl4 and vehicle injections; and d) CCl4+P = mice subjected to CCl4 and pamidronate injections. CCl4 or vehicle was administered for 8 weeks, while pamidronate or vehicle was injected at the end of the fourth week. Bone histomorphometry and biomechanical analysis were performed in tibiae, while femora were used for micro-computed tomography and gene expression. RESULTS:: CCl4 mice exhibited decreased bone volume/trabecular volume and trabecular numbers, as well as increased trabecular separation, as determined by bone histomorphometry and micro-computed tomography, but these changes were not detected in the group treated with pamidronate. CCl4 mice showed increased numbers of osteoclasts and resorption surface. High serum levels of receptor activator of nuclear factor-κB ligand and the increased expression of tartrate-resistant acid phosphatase in the bones of CCl4 mice supported the enhancement of bone resorption in these mice. CONCLUSION:: Taken together, these results suggest that bone resorption is the main mechanism of bone loss in chronic hepatocellular disease in mice.

Hepatic Osteodystrophy: The Mechanism of Bone Loss in Hepatocellular Disease and the Effects of Pamidronate Treatment

OBJECTIVES: The present study was designed to evaluate the bone phenotypes and mechanisms involved in bone disorders associated with hepatic osteodystrophy. Hepatocellular disease was induced by carbon tetrachloride (CCl4). In addition, the effects of disodium pamidronate on bone tissue were evaluated. METHODS: The study included 4 groups of 15 mice: a) C = mice subjected to vehicle injections; b) C+P = mice subjected to vehicle and pamidronate injections; c) CCl4+V = mice subjected to CCl4 and vehicle injections; and d) CCl4+P = mice subjected to CCl4 and pamidronate injections. CCl4 or vehicle was administered for 8 weeks, while pamidronate or vehicle was injected at the end of the fourth week. Bone histomorphometry and biomechanical analysis were performed in tibiae, while femora were used for micro-computed tomography and gene expression. RESULTS: CCl4 mice exhibited decreased bone volume/trabecular volume and trabecular numbers, as well as increased trabecular separation, as determined by bone histomorphometry and micro-computed tomography, but these changes were not detected in the group treated with pamidronate. CCl4 mice showed increased numbers of osteoclasts and resorption surface. High serum levels of receptor activator of nuclear factor-κB ligand and the increased expression of tartrate-resistant acid phosphatase in the bones of CCl4 mice supported the enhancement of bone resorption in these mice. CONCLUSION: Taken together, these results suggest that bone resorption is the main mechanism of bone loss in chronic hepatocellular disease in mice.

Fish oil decreases hepatic lipogenic genes in rats fasted and refed on a high fructose diet.

Fasting and then refeeding on a high-carbohydrate diet increases serum and hepatic triacylglycerol (TAG) concentrations compared to standard diets. Fructose is a lipogenic monosaccharide which stimulates de novo fatty acid synthesis. Omega-3 (n-3) fatty acids stimulate hepatic ß-oxidation, partitioning fatty acids away from TAG synthesis. This study investigated whether dietary n-3 fatty acids from fish oil (FO) improve the hepatic lipid metabolic response seen in rats fasted and then refed on a high-fructose diet. During the post-prandial (fed) period, rats fed a FO rich diet showed an increase in hepatic peroxisome proliferator-activated receptor α (PPAR-α) gene expression and decreased expression of carbohydrate responsive element binding protein (ChREBP), fatty acid synthase (FAS) and microsomal triglyceride transfer protein (MTTP). Feeding a FO rich diet for 7 days prior to 48 h of fasting resulted in lower hepatic TAG, lower PPAR-α expression and maintenance of hepatic n-3 fatty acid content. Refeeding on a high fructose diet promoted an increase in hepatic and serum TAG and in hepatic PPAR-α, ChREBP and MTTP expression. FO did not prevent the increase in serum and hepatic TAG after fructose refeeding, but did decrease hepatic expression of lipogenic genes and increased the n-3 fatty acid content of the liver. n-3 Fatty acids can modify some components of the hepatic lipid metabolic response to later feeding with a high fructose diet.

Low nitric oxide bioavailability is associated with better responses to sildenafil in patients with erectile dysfunction.

Erectile dysfunction (ED) is a multifactorial disease associated with vascular dysfunction, low nitric oxide (NO) bioavailability, and oxidative stress. However, it is not known whether low NO bioavailability and oxidative stress affect the responsiveness of ED patients to sildenafil. We tested this hypothesis by studying 28 healthy subjects (control group), 26 patients with ED without comorbidities (ED group), and 18 patients with ED and diabetes mellitus (ED/DM group). The International Index for Erectile Function (IIEF) questionnaire was used to assess the erectile function of all participants, and their responsiveness to sildenafil was assessed as the percentage of change in the five-item version of IIEF score before and after sildenafil treatment. Levels of whole blood nitrite, antioxidants markers (ferric reducing ability of plasma (FRAP) and reduced glutathione), and oxidative stress markers (thiobarbituric acid reactive substance and protein carbonyl) were determined. We found a negative correlation between whole blood nitrite levels and the responses to sildenafil in both ED groups (P<0.05). FRAP correlated negatively with the responses to sildenafil in the ED/DM group (P<0.05). No other significant associations were found. Our findings show evidence that low NO bioavailability is associated with better responses to sildenafil in patients with ED (with or without DM).

Oxidative-stress biomarkers in patients with pulmonary hypertension.

This controlled, prospective, nonrandomized clinical investigation has as its chief strength the fact that it was done in humans with active disease and apparently on fairly modest therapeutic regimens. The aim was to present the results of oxidative-stress biomarkers in humans suffering from pulmonary artery hypertension (PAH). Inflammation and oxidative stress are essential in PAH with increased lipid peroxidation and reduced antioxidant defenses. Twenty-four adult patients of both sexes, with a mean age of 21 years, were subdivided into 2 groups: a control group of 12 healthy, nonsmoking volunteers and a PAH group (PAHG) of 12 volunteers with PAH receiving outpatient treatment. Oxidative stress was evaluated by plasma activity of reduced glutathione (GSH); lipid peroxidation was expressed by malondialdehyde (MDA) and lipid hydroperoxide (ferrous oxidation of xylenol orange [FOX] assay); vitamin E was measured by high-performance liquid chromatography and tumor necrosis factor-α (TNF-α) by enzyme-linked immunosorbent assay. Statistical analyses showed significant differences for (1) the TNF-α measure, with highest values in PAHG patients; (2) the plasma GSH, with lowest values in PAHG patients; (3) vitamin E, with the lowest concentrations in PAHG patients; (4) MDA measure, with highest values in PAHG patients; and (5) the lipid hydroperoxide FOX measure, with highest values in PAHG patients. In conclusion, inflammation and oxidative stress are present in patients with PAH, as confirmed by increased lipid peroxidation, reduced GSH, and low concentrations of vitamin E.

Chemopreventive effects of the dietary histone deacetylase inhibitor tributyrin alone or in combination with vitamin A during the promotion phase of rat hepatocarcinogenesis.

The chemopreventive effects of tributyrin (TB) and vitamin A (VA), alone or in combination, were investigated during the promotion phase of rat hepatocarcinogenesis. Compared to diethylnitrosamine control rats, TB and TB+VA-treated rats, but not VA-treated rats, presented a lower incidence and mean number of hepatocyte nodules and a smaller size of persistent preneoplastic lesions (pPNLs). In addition, TB and TB+VA-treated rats exhibited a higher apoptotic body index in pPNL and remodeling PNL, whereas VA-treated rats presented only a higher apoptotic body index in remodeling PNL. None of the treatments inhibited cell proliferation in PNL. TB and TB+VA-treated rats, but not VA-treated rats, exhibited higher levels of H3K9 acetylation and p21 protein expression. TB and VA-treated rats exhibited increased hepatic concentrations of butyric acid and retinoids, respectively. Compared to normal rats, diethylnitrosamine control animals exhibited lower retinyl palmitate hepatic concentrations. All groups had similar expression levels and exhibited similar unmethylated CRBP-I promoter region in microdissected pPNL, indicating that epigenetic silencing of this gene was not involved in alteration of retinol metabolism in early hepatocarcinogenesis. Data support the effectiveness of TB as a dietary histone deacetylase inhibitor during the promotion phase of hepatocarcinogenesis, which should be considered for chemoprevention combination strategies.

Oxidative stress biomarker responses to an acute session of hypertrophy-resistance traditional interval training and circuit training.

We have studied circuit resistance schemes with high loads as a time-effective alternative to hypertrophy-traditional resistance training. However, the oxidative stress biomarker responses to high-load circuit training are unknown. The aim of the present study was to compare oxidative stress biomarker response with an acute session of hypertrophy-resistance circuit training and traditional interval training. A week after the 1 repetition maximum (1RM) test, 11 healthy and well-trained male participants completed hypertrophy-resistance acute sessions of traditional interval training (3 × 10 repetitions at 75% of the 1RM, with 90-second passive rest) and circuit training (3 × 10 repetitions at 75% of the 1RM, in alternating performance of 2 exercises with different muscle groups) in a randomized and cross-over design. Venous blood samples were collected before (pre) and 10 minutes after (post) the resistance training sessions for oxidative stress biomarker assays. As expected, the time used to complete the circuit training (20.2 ± 1.6) was half of that needed to complete the traditional interval training (40.3 ± 1.8). Significant increases (p < 0.05) in thiobarbituric acid reactive substances (40%), creatine kinase (CK) (67%), glutathione (14%), and uric acid (25%) were detected posttraditional interval training session in relation to pre. In relation to circuit training, a significant increase in CK (33%) activity postsession in relation to pre was observed. Statistical analysis did not reveal any other change in the oxidative stress biomarker after circuit training. In conclusion, circuit resistance-hypertrophy training scheme proposed in the current study promoted lower oxidative stress biomarkers and antioxidant modulations compared with resistance traditional interval training.

Antioxidant effect of thiamine on acutely alcoholized rats and lack of efficacy using thiamine or glucose to reduce blood alcohol content.

Although there is no consensus about the use of glucose and thiamine for the treatment of acute ethanol intoxication, this is a routine practice in many countries. Our objective was to determine the efficacy of this treatment and the changes it causes in the antioxidant status of the liver. Male Wistar rats were intoxicated with an ethanol dose of 5 g/kg and divided into three groups: ethanol (EtOH; untreated), EtOH+G (treated with glucose), and EtOH+B1 (treated with thiamine). Blood and urinary ethanol as well as hepatic malondialdehyde, reduced glutathione and vitamin E were determined in all animals. Blood alcohol levels did not differ between groups, although urinary excretion was about four times higher in the group treated with thiamine (EtOH+B1). The malondialdehyde, reduced glutathione and vitamin E values used here as parameters of the antioxidant system of the liver showed improvement for the thiamine-treated group (EtOH+B1). Treatment with glucose or thiamine was ineffective in reducing blood alcohol levels in rats with acute ethanol intoxication. However, the beneficial effect of thiamine as an antioxidant for ethanol metabolism was demonstrated. Further investigations are necessary to clarify the urinary excretion of ethanol reported here for the first time and the possibility of using thiamine as an antioxidant in situations of chronic alcohol use.

The protective effect of CAPE on hepatic ischemia/reperfusion injury in rats.

BACKGROUND/AIMS: The transcription factor nuclear factor-kappa B (NF-kappaB) exerts a pivotal role in the pathogenesis of hepatic ischemia/reperfusion (I/R) injury. Caffeic acid phenyl ester (CAPE), a potent and specific NF-kappaB inhibitor, presents protective effects on I/R injury in some tissues. This study aimed to evaluate the effect of CAPE on hepatic I/R injury in rats. MATERIALS AND METHODS: Wistar rats were submitted to a sham operation, 60 min ischemia, or 60 min ischemia plus saline or CAPE treatment followed by 6 h reperfusion. Liver tissue injury was evaluated by alanine aminotransferase, aspartate aminotransferase, and tissue glutathione measurement, and histological damage score. Apoptotic hepatocytes were determined by the transferase-mediated dUTP-biotin nick-end labeling assay. Hepatic neutrophil accumulation was assessed by the naphthol method. Lipid peroxidation and NF-kappaB activation were evaluated by 4-hydroxynonenal and NF-kappaB p65 immunohistochemistry, respectively. RESULTS: Animals submitted to ischemia showed a marked increase of alanine aminotransferase and aspartate aminotransferase after reperfusion, but with lower levels in CAPE group. Tissue glutathione content declined gradually during ischemia to reperfusion and was partially recovered with CAPE treatment. The histological damage score, apoptosis index, and neutrophil infiltration, as well as 4-hydroxynonenal and NF-kappaB p65 nuclear labeling, were higher in the liver of animals submitted to I/R compared to the ischemia group. However, the CAPE treatment significantly reduced all of these alterations. CONCLUSIONS: CAPE was able to protect the liver against normothermic I/R injury in rats. This effect may be associated with the inhibition of the NF-kappaB signaling pathway and decrease of the acute inflammatory response following I/R in the liver.

Suplementação de creatina, homocisteínae estresse oxidativo / Creatine supplementation, homocysteine and oxidative stress

A creatina é uma substância popular entre atletas devido a sua possível propriedade ergogênica. Tal popularidade incentivou autores a estudar e explorar o possível potencial terapêutico desta substância. A síntese de creatina é responsável pela maioria das transferências de grupos metila no metabolismo hepático normal. Como a homocisteína é um aminoácido formado exclusivamente a partir da desmetilação da metionina, acredita-se que a creatina e homocisteína estejam metabolicamente conectadas. Estudos têm mostrado que a hiperhomocisteinemia está diretamente ligada à formação de espécies reativas de oxigênio pela auto oxidação da homocisteína e/ou da cisteína e que tal auto-oxidação pode provocar danos celulares.O objetivo desta revisão é discutir aspectos da suplementação com creatina relacionados aos níveis de homocisteína e o estresse oxidativo.

Creatine is a popular substance among athletes due its possible ergogenic property. Such popularity has been stimulating authors to study and explore the possible potencial therapeutic effect of this substance. The synthesis of creatine is responsible for the majority methyl groups transferences in the normal hepatic metabolism. As homocysteine is an aminoacid formed exclusively from the methionine demetilation, it is believed that creatine and homocysteine are metabolically connected. Studies have show that hyperhomocysteinemia is directly linked tooxygen reactive species formation by the homocysteine and/or cysteine auto-oxidation and this can promote cellular damage. The aim of this review is to discuss some aspects of creatine supplementation on homocysteine levels and oxidative stress.

Influence of thyroid hormone on thyroid hormone receptor beta-1 expression and lacrimal gland and ocular surface morphology.

PURPOSE: Hormone diseases induce changes in the lacrimal gland (LG) and ocular surface (OS). Thyroid hormone (TH) induces cell proliferation and lipid metabolism through the activation of TH receptors. The aim of the present study was to evaluate the location and comparative expression of TH receptor beta-1 (Thrb) in LG of rats with hypothyroidism and in controls and to evaluate the impact of this disease on LG and OS structure and function. METHODS: Hypothyroidism was induced in Wistar male rats by the long-term use of tiamazole. Ten weeks later corneal cells were collected for impression cytology (IC). Rats were humanely killed, and tissues were evaluated by immunoperoxidase staining and Western blot for Thrb. The content of malondialdehyde (MDA) and acetylcholine (ACh) in LG was determined by spectrophotometry (n = 5/group in all experiments). RESULTS: LG weight was significantly lower in hypothyroid rats (P < 0.05). Western blot analysis indicated that LGs express Thrb and that hypothyroidism induces a higher expression of this receptor. IC was significantly different and ACh was significantly lower in hypothyroid rats (P < 0.05). CONCLUSIONS: Chronically reduced levels of TH lead to biochemical and structural changes and modulate the levels of Thrb in LG. These events confirm that LG is a target organ for TH and may facilitate understanding of the mechanism related to dry eye in hypothyroidism.

[Prevalence of iron deficiency and its association with vitamin A deficiency in preschool children]. / Prevalência da carência de ferro e sua associação com a deficiência de vitamina A em pré-escolares.

OBJECTIVES: To identify the prevalence of iron deficiency in the population studied, as well as verifying if such deprivation is associated with vitamin A deficiency. METHODS: One hundred seventy-nine children, > or = 24 months and < 72 months of age, with no diarrhea and/or fever at collection were studied. Vitamin A deficiency identification was carried out through serum 30-day dose-response test. Samples of peripheral blood from fasting children was obtained for hemoglobin counts, serum iron, and unsaturated iron binding capacity assays. Information about the presence of diarrhea and/or fever during the 15 days preceding the study was also obtained. RESULTS: 35.8% (64/179) of the children presented iron deficiency and 75.4% (135/179), vitamin A deficiency. 29.1% (52/179) of the children presented both iron and vitamin A deficiencies. Iron deficiency was not associated with vitamin A deficiency. A separate analysis for each hematimetric index also demonstrated no significant difference between children with or without vitamin A deficiency. Children aged 24 to 36 months presented significantly higher prevalence rates of iron deficiency (p = 0.0005) as did children with diarrhea and/or fever during the 15 days preceding the study (p = 0.003). CONCLUSIONS: Although iron deficiency was not associated with vitamin A deficiency, high rates of both deficiencies were exhibited in a "healthy" population with low malnutrition indices. Such situations are known as "hidden hunger". Younger children presented a higher risk of iron deficiency as did children with diarrhea and/or fever during the 15 days preceding the study.

Niacin metabolite excretion in alcoholic pellagra and AIDS patients with and without diarrhea.

OBJECTIVE: Malnourished patients with the acquired immunodeficiency syndrome (AIDS) can develop pellagra-like manifestations such as dermatitis, diarrhea, and dementia; therefore, we tested the hypothesis that patients with AIDS and diarrhea would have niacin depletion. This study compared 24-h urine excretion of N1-methyl-nicotinamide (N1MN) among patients with pellagra and patients with AIDS who did and did not have diarrhea. METHODS: Three groups were studied: G1 (patients with AIDS and diarrhea, n = 5); G2 (patients with AIDS and no diarrhea, n = 7), and G3 (patients with alcoholic pellagra and without the human immunodeficiency virus, n = 8). Diarrhea was defined as the production of at least three liquid stools per day over 3 to 5 d. Studies included mucosal intestinal biopsy, malabsorption tests, detection of parasites in stool, and serum albumin measurements. Semiquantitative food-frequency questionnaire, anthropometry, and daily urinary N1MN excretion were also determined. Groups were matched in relation to age, sex, presence of parasites in stool, and intestinal absorption results. RESULTS: G1 had normal intestinal examination by light microscopy and no parasites in stools. G2 group showed lower levels of serum albumin (2.6 +/- 0.3 g/dL) when compared with G1 (3.4 +/- 0.3 g/dL) and G3 (3.1 +/- 0.7 g/dL). Except for patients with pellagra, groups met their energy requirements. Patients in G3 (0.013, 0.01-0.081 mg/dL) and G1 (0.062, 0.001-0.33 mg/dL) excreted smaller amounts of N1MN in urine than did those in G2 (0.63, 0.02-2.9 mg/dL). CONCLUSIONS: Patients with AIDS and diarrhea excreted less N1MN in urine than did those without diarrhea. These patients may have an impaired niacin nutritional status, possibly associated with increased metabolic needs.