Bio-efficacy of iron and zinc fortified wheat flour along with bio-assessment of its hepatic and renal toxic potential / Bioeficácia da farinha de trigo fortificada com ferro e zinco e bioavaliação do seu potencial tóxico hepático e renal

Study was planned to assess the bio-efficiency along with toxicity of iron and zinc fortified whole wheat flour in Sprague dawley albino rats. Whole wheat flour was fortified with different dosage of sodium iron EDTA (NaFeEDTA), ferrous sulphate (FeSO4), zinc oxide (ZnO) and zinc sulphate (ZnSO4). The rats (n=3) in each group were fed on fortified wheat flour for 2 months. Liver biomarkers including alkaline phosphatase (ALP), alanine transaminase (ALT), aspartate aminotransferase (AST) and bilirubin were recorded from serum samples. Increased concentration of ZnSO4 affected the liver biomarkers to be highest among all whereas, bilirubin levels were less than the rats fed on control diet. The above mentioned fortificants have negligible effect on renal biomarkers including creatinine and urea. Moreover, hematological parameters were also checked and reportedly, sodium iron EDTA fed rats presented highest amount of hemoglobin, iron and total iron binding capacity. Highest zinc level was observed in rats fed on whole wheat flour fortified with 60mg/Kg Zinc oxide. Microscopic observation of liver tissue depicted that rats fed on iron and zinc fortified wheat flour have more toxic effects whereas, histopathology presentation of kidney tissue has least toxic impact. It has been concluded that mandatory fortification of wheat flour with iron and zinc may cause increased serum biomarkers along with toxicity of vital organs like liver, hence fraction of wheat flour may be fortified to fulfill the requirements of deprived and vulnerable group.

O estudo foi planejado para avaliar a bioeficiência juntamente com a toxicidade da farinha de trigo integral fortificada com ferro e zinco em ratos albinos Sprague dawley. A farinha de trigo integral foi fortificada com diferentes dosagens de ferro sódico EDTA (NaFeEDTA), sulfato ferroso (FeSO4), óxido de zinco (ZnO) e sulfato de zinco (ZnSO4). Os ratos (n = 3) de cada grupo foram alimentados com farinha de trigo fortificada por 2 meses. Biomarcadores hepáticos incluindo fosfatase alcalina (ALP), alanina transaminase (ALT), aspartato aminotransferase (AST) e bilirrubina foram registrados a partir de amostras de soro. O aumento da concentração de ZnSO4 afetou os biomarcadores hepáticos como sendo os mais altos entre todos, enquanto os níveis de bilirrubina foram menores do que os ratos alimentados com dieta controle. Os fortificantes mencionados acima têm efeito insignificante nos biomarcadores renais, incluindo creatinina e ureia. Além disso, os parâmetros hematológicos também foram verificados e, segundo relatos, os ratos alimentados com EDTA de sódio e ferro apresentaram maior quantidade de hemoglobina, ferro e capacidade total de ligação de ferro. O maior nível de zinco foi observado em ratos alimentados com farinha de trigo integral fortificada com 60 mg/Kg de óxido de zinco. A observação microscópica do tecido hepático mostrou que ratos alimentados com farinha de trigo fortificada com ferro e zinco têm mais efeitos tóxicos, enquanto a apresentação histopatológica do tecido renal tem menos impacto tóxico. Concluiu-se que a fortificação obrigatória da farinha de trigo com ferro e zinco pode causar aumento dos biomarcadores séricos juntamente com toxicidade de órgãos vitais como o fígado, portanto a fração da farinha de trigo pode ser fortificada para atender os requisitos do grupo carente e vulnerável.

Histomorphometric and immunohistochemical evaluation of the frontal cerebral cortex in diabetic rats after treatment with melatonin / Avaliação histomorfométrica e imuno-histoquímica do córtex cerebral frontal em ratos diabéticos após o tratamento com melatonina

The central nervous system is vulnerable to complications caused by diabetes. These complications lead to increased oxidative stress in the brain, resulting in damage to the cerebral cortex, among other regions. Insulin and hypoglycemic agents are still the most widely used treatments. However, current research with an experimental model of diabetes suggests the use of antioxidants, such as melatonin. Thus, we tested the hypothesis that exogenous melatonin may decrease or prevent the effects of diabetes in the frontal cortex of the rat brain. Fifty albino rats were allocated into five groups: GC = rats without diabetes induction, GD = diabetic rats induced by streptozotocin, GDM = streptozotocin-induced and melatonin-treated diabetic rats, GDI = diabetic rats induced by streptozotocin and treated with insulin, GDMI = diabetic rats induced by streptozotocin and treated with melatonin and insulin simultaneously. Diabetes was induced by intraperitoneal administration of streptozotocin (60mg/kg). Insulin (5U/day) was administered subcutaneously and melatonin (10mg/kg) by drinking water; both treatments last days after. We analyzed animals' weight, the cytokines IL-6 and TNF-α, apoptosis, glycogen, and did morphometry and histopathology of the frontal cortex were analyzed. The results showed that the cerebral cortex of the diabetic animals presented axonal degeneration, reduced number of neurons in the cortex, reduced glycogen, increased IL-6 and TNF-α expression, high apoptotic index, and reduced animal weight and the brain. Treatment with melatonin associated or not with insulin prevented such effects. Thus, we conclude that melatonin associated with insulin may be an alternative for avoiding the impact of diabetes in the brain's frontal cortex.(AU)

O sistema nervoso central é vulnerável a complicações originadas pelo diabetes estresse oxidativo no cérebro e resultando em lesões no córtex cerebral, dentre outras regiões. A insulina e hipoglicemiantes ainda são os tratamentos mais utilizados, entretanto, pesquisas atuais com modelo experimental do diabetes sugerem a utilização de antioxidantes como, por exemplo, a melatonina. Assim, testamos a hipótese de que a melatonina exógena pode diminuir ou prevenir os efeitos do diabetes no córtex frontal do cérebro de ratos. Foram utilizados 50 ratos albinos, divididos em 5 grupos: GC = ratos sem indução ao diabetes, GD = ratos induzidos ao diabetes pela estreptozotocina, GDM = ratos induzidos ao diabetes pela estreptozotocina e tratados com melatonina, GDI = ratos induzidos ao diabetes pela estreptozotocina e tratados com insulina, GDMI = ratos induzidos ao diabetes pela estreptozotocina e tratados com melatonina e insulina simultaneamente. O diabetes foi induzido pela administração intraperitoneal de estreptozotocina (60mg/kg). A insulina (5U/dia) foi administrada por via subcutânea e a melatonina (10mg/kg) pela água de beber. Ambos tratamentos foram realizados durante 30 dias após a indução. Foram analisados o peso dos animais, do cerebro, as citocinas IL-6 e TNF-α, apoptose, glicogênio, além da morfometria e histopatologia do córtex frontal. Os resultados mostraram que o córtex cerebral dos animais diabéticos apresentou degeneração axonal, redução do número de neurônios no córtex, redução do glicogênio, aumento da expressão do IL-6 e TNF-α, elevação do índice apoptótico, além da redução do peso dos animais e do cérebro. O tratamento com melatonina associada ou não a insulina preveniu tais efeitos. Assim, concluímos que a melatonina associada ou não a insulina pode ser uma alternativa na prevenção dos efeitos do diabetes no córtex frontal do cérebro.(AU)

Histomorphometric and immunohistochemical evaluation of the frontal cerebral cortex in diabetic rats after treatment with melatonin / Avaliação histomorfométrica e imuno-histoquímica do córtex cerebral frontal em ratos diabéticos após o tratamento com melatonina

The central nervous system is vulnerable to complications caused by diabetes. These complications lead to increased oxidative stress in the brain, resulting in damage to the cerebral cortex, among other regions. Insulin and hypoglycemic agents are still the most widely used treatments. However, current research with an experimental model of diabetes suggests the use of antioxidants, such as melatonin. Thus, we tested the hypothesis that exogenous melatonin may decrease or prevent the effects of diabetes in the frontal cortex of the rat brain. Fifty albino rats were allocated into five groups: GC = rats without diabetes induction, GD = diabetic rats induced by streptozotocin, GDM = streptozotocin-induced and melatonin-treated diabetic rats, GDI = diabetic rats induced by streptozotocin and treated with insulin, GDMI = diabetic rats induced by streptozotocin and treated with melatonin and insulin simultaneously. Diabetes was induced by intraperitoneal administration of streptozotocin (60mg/kg). Insulin (5U/day) was administered subcutaneously and melatonin (10mg/kg) by drinking water; both treatments last days after. We analyzed animals' weight, the cytokines IL-6 and TNF-α, apoptosis, glycogen, and did morphometry and histopathology of the frontal cortex were analyzed. The results showed that the cerebral cortex of the diabetic animals presented axonal degeneration, reduced number of neurons in the cortex, reduced glycogen, increased IL-6 and TNF-α expression, high apoptotic index, and reduced animal weight and the brain. Treatment with melatonin associated or not with insulin prevented such effects. Thus, we conclude that melatonin associated with insulin may be an alternative for avoiding the impact of diabetes in the brain's frontal cortex.(AU)

O sistema nervoso central é vulnerável a complicações originadas pelo diabetes estresse oxidativo no cérebro e resultando em lesões no córtex cerebral, dentre outras regiões. A insulina e hipoglicemiantes ainda são os tratamentos mais utilizados, entretanto, pesquisas atuais com modelo experimental do diabetes sugerem a utilização de antioxidantes como, por exemplo, a melatonina. Assim, testamos a hipótese de que a melatonina exógena pode diminuir ou prevenir os efeitos do diabetes no córtex frontal do cérebro de ratos. Foram utilizados 50 ratos albinos, divididos em 5 grupos: GC = ratos sem indução ao diabetes, GD = ratos induzidos ao diabetes pela estreptozotocina, GDM = ratos induzidos ao diabetes pela estreptozotocina e tratados com melatonina, GDI = ratos induzidos ao diabetes pela estreptozotocina e tratados com insulina, GDMI = ratos induzidos ao diabetes pela estreptozotocina e tratados com melatonina e insulina simultaneamente. O diabetes foi induzido pela administração intraperitoneal de estreptozotocina (60mg/kg). A insulina (5U/dia) foi administrada por via subcutânea e a melatonina (10mg/kg) pela água de beber. Ambos tratamentos foram realizados durante 30 dias após a indução. Foram analisados o peso dos animais, do cerebro, as citocinas IL-6 e TNF-α, apoptose, glicogênio, além da morfometria e histopatologia do córtex frontal. Os resultados mostraram que o córtex cerebral dos animais diabéticos apresentou degeneração axonal, redução do número de neurônios no córtex, redução do glicogênio, aumento da expressão do IL-6 e TNF-α, elevação do índice apoptótico, além da redução do peso dos animais e do cérebro. O tratamento com melatonina associada ou não a insulina preveniu tais efeitos. Assim, concluímos que a melatonina associada ou não a insulina pode ser uma alternativa na prevenção dos efeitos do diabetes no córtex frontal do cérebro.(AU)

Anabolic-androgenic steroids cycle administration decreases anxious-like behavior but does not affect long-term memory acquisition in rats

The steroid hormones are lipids in nature, which play crucial roles in several metabolic and behavioral pathways in mammals. Drug therapy uses sterol hormones for treating some disturbances linked with its deficiency; however, the illicit use of these hormones by amateur and elite athletes to enhance performance or body appearance may lead to several health issues. In this study we evaluated the anxious-like behavior and the long-term memory acquisition of male rats undergoing sedentary life-style or physical effort, with or without anabolic-androgenic steroids (ASC) treatment. The results showed a decrease in anxious-like behavioral levels in rats that received ASC treatment associated or not with physical effort, but this treatment did not affect the acquisition of long-term memory at the dose and experimental model assessed.

Anabolic-androgenic steroids cycle administration decreases anxious-like behavior but does not affect long-term memory acquisition in rats

The steroid hormones are lipids in nature, which play crucial roles in several metabolic and behavioral pathways in mammals. Drug therapy uses sterol hormones for treating some disturbances linked with its deficiency; however, the illicit use of these hormones by amateur and elite athletes to enhance performance or body appearance may lead to several health issues. In this study we evaluated the anxious-like behavior and the long-term memory acquisition of male rats undergoing sedentary life-style or physical effort, with or without anabolic-androgenic steroids (ASC) treatment. The results showed a decrease in anxious-like behavioral levels in rats that received ASC treatment associated or not with physical effort, but this treatment did not affect the acquisition of long-term memory at the dose and experimental model assessed.(AU)

GDF11 ameliorated myocardial ischemia reperfusion injury by antioxidant stress and up-regulating autophagy in STZ-induced type 1 diabetic rats

Purpose: To investigate whether GDF11 ameliorates myocardial ischemia reperfusion (MIR) injury in diabetic rats and explore the underlying mechanisms. Methods: Diabetic and non-diabetic rats subjected to MIR (30 min of coronary artery occlusion followed by 120 min of reperfusion) with/without GDF11 pretreatment. Cardiac function, myocardial infarct size, creatine kinase-MB (CK-MB), lactate dehydrogenase (LDH), superoxide dismutase (SOD) 15-F2tisoprostane, autophagosome, LC3II/I ratio and Belcin-1 level were determined to reflect myocardial injury, oxidative stress and autophagy, respectively. In in vitro study, H9c2 cells cultured in high glucose (HG, 30mM) suffered hypoxia reoxygenation (HR) with/without GDF11, hydrogen peroxide (H2O2) and autophagy inhibitor 3-methyladenine (3-MA) treatment, cell injury; oxidative stress and autophagy were assessed. Results: Pretreatment with GDF11 significantly improved cardiac morphology and function in diabetes, concomitant with decreased arrhythmia severity, infarct size, CK-MB, LDH and 15-F2tisoprostane release, increased SOD activity and autophagy level. In addition, GDF11 notably reduced HR injury in H9c2 cells with HG exposure, accompanied by oxidative stress reduction and autophagy up-regulation. However, those effects were completely reversed by H2O2 and 3-MA. Conclusion: GDF11 can provide protection against MIR injury in diabetic rats, and is implicated in antioxidant stress and autophagy up-regulation.(AU)

Dexmedetomidine protects against renal ischemia and reperfusion injury by inhibiting the P38-MAPK/TXNIP signaling activation in streptozotocin induced diabetic rats

Purpose: To determine whether dexmedetomidine (DEX) could attenuate acute kidney injury (AKI) induced by ischemia/reperfusion (I/R) in streptozotocin (STZ)-induced diabetic rats. Methods: Four groups each containing six rats were created (sham control(S), diabetes-sham (DS), diabetes I/R (DI/R), and diabetes-I/R-dexmedetomidine (DI/R-DEX). In diabetes groups, single-dose (65 mg/kg) STZ was administered intraperitoneally (i.p.). In Group DI/R, ischemia reperfusion was produced via 25 min of bilateral renal pedicle clamping followed by 48 h of reperfusion. In Group DI/R-DEX, 50 g/kg dexmedetomidine was administered intraperitoneally 30 minutes before ischemia. Renal function, histology, apoptosis, the levels of TNF-, IL-1, and oxidative stress in diabetic kidney were determined. Moreover, expression of P38 mitogen-activated protein kinase (P38-MAPK), phosphorylated-P38-MAPK(p-P38-MAPK) and thioredoxin-interacting protein (TXNIP) were assessed. Results: The degree of renal I/R injury was significantly increased in DI/R group compared with S group and DS group. The levels of TNF-, IL-1, oxidative stress and apoptosis were found significantly higher in DI/R Group when compared with S Group and DS Group. The protein expression of p-P38-MAPK and TXNIP were significantly increased after I/R. All these changes were reversed by DEX treatment. Conclusion: The renoprotective effects of DEX-pretreatment which attenuates I/R-induced AKI were partly through inhibition of P38-MAPK activation and expression of TXINP in diabetic kidney.(AU)

The role of ischemic preconditioning and pentoxifylline in intestinal ischemia/reperfusion injury of rats

Purpose: To investigate the role of ischemic preconditioning (IPC) and pentoxifylline (PTX) in intestinal mucosa ischemia/reperfusion injury (IR). Methods: Thirty rats were assigned to 5 groups (N=6): (CG): no clamping of the superior mesenteric artery (90 min.); (IR-SS): saline + ischemia (30 min.) + reperfusion (60 min.); (IR-PTX): PTX + ischemia (30min.) + reperfusion (60 min.); (IPC-IR-SS): 5 min. of ischemia + 5 minutes of reperfusion (IPC) + saline + ischemia (30 min.) + reperfusion (60 min.); (IPC-IR-PTX ): 5 min. of ischemia + 5 min. of reperfusion (IPC) + PTX + 30 min. of I + 60 minutes of R. Results: The IR-PTX, IPC-IR-SS and IPC-IR-PTX groups had significantly lower scores of mucosa damage than the IR-SS group. IR-PTX group showed higher scores than the IPC-IR-PTX group, in accordance with the hypothesis of a favorable effect of IPC alone or in association with PTX. Additionally, IPC-IR-SS had a higher damage score than the IPC-IR-PTX. The villi height and crypt depth were similar in all groups. The villi height in the IR-SS was significantly lower. Conclusion: Ischemic preconditioning or pentoxifylline alone protect the intestinal mucosa from ischemia/reperfusion injury. However, they do not have a synergistic effect when applied together.(AU)

Evaluation of silybum marinaum efficacy on University of Wisconsin and histidine-tryptophan-ketoglutarate solutions latter the damage of the perfused liver

Purpose: To investigate the hepatoprotective and antioxidant effeicacies of Silybum marianums (silymarin, S) on University of Wisconsin (UW) and histidinetryptophan-ketoglutarate (HTK) preservation solutions. Methods: Thirty two Wistar albino adult male rats were used. Group 1: UW group, Group 2: UW + Silymarin group(S), Group 3: HTK group, Group 4: HTK + silymarin group (S), respectively. Silymarin was enforced intraperitoneally before the surgery. Biopsies were enforced in 0, 6 and 12.hours to investigate. Results: Biochemical parameters examined in alanine aminotransferase (ALT), furthermore superoxide dismutase (SOD), catalase (CAT), and malondialdehyde (MDA) in rats were also evaluated. Detected histopathological changings were substantially declining in the groups that received silymarin, cellular damage was decreased significantly in HTK + Silymarin group, according to other groups. It has been identified as the most effective group was HTK + silymarin group in evaluation of ALT, electron microscopic results, also decreased MDA and elevated in SOD, and CAT activity. Caspase 3 analysis showed a substantial lower apoptosis ratio in the silymarin groups than in the non-performed groups (p 0.05). Conclusion: Histidinetryptophan-ketoglutarate+silymarin group provides better hepatoprotection than other groups, by decreasing the hepatic pathologic damage, delayed changes that arise under cold ischemic terms.(AU)

Fluorescent test accurately predicts leak of ischemic colon anastomosis in rats

Purpose: To investigate if fluorescein fluorescent test can predict dehiscence in a model of ischemic colonic anastomosis in rats. Methods: This experimental controlled trial randomly assigned 55 rats to four groups. Anastomoses were performed in non-ischemic colon segments (control group) and in ischemic colon segments measuring 1, 2 or 3 cm long (groups 1, 2 and 3, respectively). Fluorescein was injected and the tissues were examined under ultraviolet light. Seven days later, a second-look surgery was performed to check for the presence or absence of anastomosis dehiscence. Results: Twenty-four rats presented anastomotic dehiscence during the second-look surgery. Reticular and nonfluorescent patterns were significantly associated with the occurrence of anastomotic dehiscence. Fluorescein fluorescence had a sensitivity of 95.8%, specificity of 89.2%, positive predictive value of 88.4%, negative predictive value of 96.2%, and accuracy of 92.3% to predict anastomotic dehiscence. Conclusion: Fluorescein fluorescent test can accurately predict leak in a model of ischemic colonic anastomosis in rats.(AU)

Automated method and not automated: the evaluation of hematological parameters of rats / Método automatizado e não automatizado:na avaliação dos parâmetros hematológicos de ratos

The aim of this study was to verify blood compatibility between automated and non-automated methodology in rats. Counts were made of haematological variables 10 Wistar rat, Rattus norvegicus. For the automated method were used the ABX-Pentra-60c + equipment and Celldyn-3200. For non-automated method the hemocytometer was used, the counts of erythrocytes, leukocytes and platelets using the liquid Hayem (1: 200), the liquid Türker (1:20) and the liquid Brecher and Conqrite (1: 200), respectively. The determination of the hematocrit was obtained using a microhematocrit centrifuge, hemoglobin concentration by cyanmethaemoglobin method (Drabkin liquid) and absolute RBC indices, calculated by the results of red series. The differential leukocyte count was performed on blood extensions (fast Panotic). Data were analyzed by analysis of variance - ANOVA followed by Tukey test at 5% significance level. The values obtained by hemocytometer compared to hematological counters showed significant differences (p 0.05) for neutrophils, eosinophils and basophils. The results showed that the counts made with the devices used were reliable and fast, but are not indicated for the differential count of white blood cell.(AU)

O objetivo deste trabalho foi verificar em sangue de rato a compatibilidade entre a metodologia automatizada e a não automatizada.Foram realizadas contagens das variáveis hematológicas de 10 ratos Wistar, Rattus norvegicus. Para o método automatizadoforam utilizados os aparelhos ABX-Pentra-60c+ e Celldyn-3200. Para o método não automatizado foi utilizado o hemocitômetronas contagens de eritrócitos, de leucócitos e de plaquetas, utilizando o líquido de Hayem (1:200), o líquido de Türk (1:20) e olíquido de Brecher e Cronkite (1:200), respectivamente. A determinação do hematócrito foi obtida utilizando-se uma centrífugade micro-hematócrito, a concentração de hemoglobina pelo método de cianometa-hemoglobina (líquido de Drabkin) e os índiceshematimétricos absolutos calculados através dos resultados da série vermelha. A contagem diferencial de leucócitos foi realizadaem extensões de sangue (panótico rápido). Os dados foram analisados através da variância ANOVA, seguida pelo teste Tukey,com nível de significância de 5%. Os valores obtidos pelo hemocitômetro comparadas aos contadores hematológicos mostraramdiferenças significativas (p < 0,05) para neutrófilos, eosinófilos e basófilos. Os resultados permitiram concluir que as contagensrealizadas com os aparelhos utilizados foram confiáveis e rápidas, mas não são indicadas para a contagem diferencial de leucócito.(AU)

Heat shock proteins (HSP)-60, -70, -90, and 105 display variable spatial and temporal immunolocalization patterns in the involuting rat uterus

Uterine involution involves substantial tissue destruction and subsequent repair and remodelling, with similarities to the microenvironments present during wound healing. Although involution is a physiologically normal process, it may generate a stressful microenvironment for the uterine cells, and thus it can induce the expression of heat shock proteins (HSPs), which were originally identified as stress-responsive proteins. The aim of this study was to determine the spatial and temporal expression and localization of four heat shock proteins (HSPD1/HSP60, HSPA/HSP70, HSPC/HSP90 and HSPH1/HSP105/110) in the involuting rat uterus using immunohistochemistry. The HSPs were expressed in the luminal (LE) and glandular epithelium (GE), fibroblasts, mast cells, myometrial myocytes, perimetrial mesothelium and blood vessels, and each of the uterine tissues had distinctive patterns of HSP immunostaining. HSPD1/HSP60 was located in the cytoplasm, often with the granular appearance that is typical of organellar localization, whereas HSPA/HSP70, HSPC/HSP90 and HSPH1/HSP105 were located in the nucleus and cytoplasm. The immunolocalization patterns of all HSPs in the LE showed alterations that accompanied involution, but no difference was observed in the other uterine cells. HSPs were localized in the apical and basal cytoplasm of the LE on postpartum days 1, 5 and 10, but only in the apical cytoplasm on day 3. Furthermore, on day 3, HSPA/HSP70, HSPC/HSP90 and HSPH1/HSP105 immunostaining in the crypts and GE were stronger than those in the LE, whereas on day 10, the nuclear HSP90 immunoreaction was stronger in the LE than in the GE. These observations suggest that HSPs may be involved in many physiological processes, such as cell cycle control, cell proliferation, regulation of cell death and survival, and differentiation during the involution process.

Heat shock proteins (HSP)-60, -70, -90, and 105 display variable spatial and temporal immunolocalization patterns in the involuting rat uterus

Uterine involution involves substantial tissue destruction and subsequent repair and remodelling, with similarities to the microenvironments present during wound healing. Although involution is a physiologically normal process, it may generate a stressful microenvironment for the uterine cells, and thus it can induce the expression of heat shock proteins (HSPs), which were originally identified as stress-responsive proteins. The aim of this study was to determine the spatial and temporal expression and localization of four heat shock proteins (HSPD1/HSP60, HSPA/HSP70, HSPC/HSP90 and HSPH1/HSP105/110) in the involuting rat uterus using immunohistochemistry. The HSPs were expressed in the luminal (LE) and glandular epithelium (GE), fibroblasts, mast cells, myometrial myocytes, perimetrial mesothelium and blood vessels, and each of the uterine tissues had distinctive patterns of HSP immunostaining. HSPD1/HSP60 was located in the cytoplasm, often with the granular appearance that is typical of organellar localization, whereas HSPA/HSP70, HSPC/HSP90 and HSPH1/HSP105 were located in the nucleus and cytoplasm. The immunolocalization patterns of all HSPs in the LE showed alterations that accompanied involution, but no difference was observed in the other uterine cells. HSPs were localized in the apical and basal cytoplasm of the LE on postpartum days 1, 5 and 10, but only in the apical cytoplasm on day 3. Furthermore, on day 3, HSPA/HSP70, HSPC/HSP90 and HSPH1/HSP105 immunostaining in the crypts and GE were stronger than those in the LE, whereas on day 10, the nuclear HSP90 immunoreaction was stronger in the LE than in the GE. These observations suggest that HSPs may be involved in many physiological processes, such as cell cycle control, cell proliferation, regulation of cell death and survival, and differentiation during the involution process.(AU)

Effects of chronic consumption of green tea on weight and body fat distribution of Wistar rats evaluated by computed tomography

Purpose: To evaluate the effects of chronic consumption of green tea on body weight and distribution of visceral fat by Computed tomography in female Wistar rats. Methods: Wistar rats were divided into control group (n = 5), which received water and feed ad libitum, and green tea group (n = 8), in which water has been replaced by green tea. The animals were weighed weekly and Computed Tomography was used at the beginning (1st week) and end (18th week) of the experiment for evaluating the distribution of visceral fat. The animals were followed for 18 weeks. Results: There was no significant difference in body weight between the groups. However, there was significant difference in visceral fat area. The green tea group had less visceral fat area at the end of the experiment, 3.67 ± 1.2 cm2, while the control group showed an area of 6.25 ± 2.2 cm (p = 0.00). Conclusions: Chronic consumption of green tea leads to decreased visceral adipose tissue area.(AU)

Effect of ovariectomy in bone structure of mandibular condyle

Purpose: To evaluate the bone structure of the mandibular condyle through an animal model, after ovariectomy. Methods: Thirty-six female Wistar rats were divided into 2 groups. The OVX group was submitted to bilateral ovariectomy, the SHAM group underwent the same surgical treatment, but without removal of the ovaries. After 90, 105 and 135 days after surgery, six animals from each group were submitted to euthanasia and the part containing the condyle was removed. Results: The microscopic analysis shows an increase in marrow spaces over time in the OVX group. The morphometric study shows reduction in the amount of bone tissue in the OVX group 135 days period in comparison with for the initial period (90 days) (p 0.05, ANOVA, Tukey). Conclusion: The estrogen deficiency also affects the bone structure of the condyle.(AU)

Perconditioning combined with postconditioning on kidney ischemia and reperfusion

Purpose: To evaluate if combination of perconditioning and postconditioning provides improved renal protection compared to perconditioning alone in a model of renal reperfusion injury. Methods: Thirty rats were assigned into 6 groups: normality; sham; ischemia and reperfusion; postconditioning; perconditioning; perconditioning + postconditioning. Animals were subjected to right nephrectomy and left renal ischemia for 30 minutes. Postconditioning consisted of 3 cycles of 5 min renal perfusion followed by 5 min of renal ischemia after major ischemic period. Perconditioning consisted of 3 cycles of 5 min hindlimb ischemia followed by 5 min of hindlimb perfusion contemporaneously to renal major ischemic period. After 24 hours, kidney was harvested and blood collected to measure urea and creatinine. Results: Perconditioning obtained better values for creatinine and urea level than only postconditioning (p 0.01); performing both techniques contemporaneously had no increased results (p>0.05). Regarding tissue structure, perconditioning was the only technique to protect the glomerulus and tubules (p 0.05), while postconditioning protected only the glomerulus (p 0.05). Combination of both techniques shows no effect on glomerulus or tubules (p>0.05). Conclusions: Perconditioning had promising results on ischemia and reperfusion induced kidney injury, enhanced kidney function and protected glomerulus and tubules. There was no additive protection when postconditioning and perconditioning were combined.(AU)

Study of the protective effect of dexamethasone on cisplatin-induced ototoxicity in rats

Purpose: To evaluate the ability of dexamethasone to protect against cisplatin (CDDP)-induced ototoxicity. Methods: Male Wistar rats were divided into the following three groups: 1) Control (C): 6 animals received intraperitoneal (IP) saline solution, 8 ml/kg/day for four days; 2) C + CDDP: 11 animals received 8 ml/kg/day of IP saline and, 90 min after saline administration, 8 mg/kg/day of IP CDDP for four days; and 3) DEXA15 + CDDP: 11 animals received IP dexamethasone 15 mg/kg/day and, 90 min after dexamethasone administration, received 8 mg/kg/day of IP CDDP for four days. Results: It was found that dexamethasone did not protect against weight loss in CDDP-exposed animals. The mortality rate was comparable with that previously reported in the literature. The auditory threshold of animals in the DEXA15 + CDDP group was not significantly altered after exposure to CDDP. The stria vascularis of animals in the DEXA15 + CDDP group was partially preserved after CDDP exposure. Conclusions: Dexamethasone at the dose of 15 mg/kg/day partially protected against CDDP-induced ototoxicity, based on functional evaluation by brainstem evoked response audiontry (BERA) and morphological evaluation by optical microscopy. However, dexamethasone did not protect against systemic toxicity.(AU)

Pulmonary oxidative stress in diabetic rats exposed to hyperoxia

Purpose: To evaluate the pulmonary oxidative stress in diabetic rats exposed to hyperoxia for 90 minutes. Methods: Forty male Wistar rats were divided into four groups, each one containing 10 animals, according to the oxygen concentration to which they were exposed: 21%, 50%, 75% and 100% (hyperoxia). In each group five animals were randomly induced to diabetes by means of at a dose of 55 mg/kg of streptozotocin (STZ). Results: Seventy two hours after diabetes induction, a significant difference was seen in blood glucose in the experimental groups in comparison with the control. In the experimental groups a significant difference was observed in the concentration of malondialdehyde (MDA) in lung tissue and blood plasma (p 0.05), except the 50% group. In the control group, significant differences in the MDA concentration in plasma and lung tissue were also observed (p 0.05), except the 75% group. The MDA concentration in lung tissue in comparison with the diabetic and non-diabetic groups showed a significant difference in the 21% group; however, no difference was seen in the 75 and 100% groups. Conclusion: In diabetic animals high oxygen concentrations (75 and 100%) do not appear to exert deleterious effects on lipid peroxidation in lung tissue.(AU)

Low-energy shock wave preconditioning reduces renal ischemic reperfusion injury caused by renal artery occlusion

Purpose: To evaluate whether low energy shock wave preconditioning could reduce renal ischemic reperfusion injury caused by renal artery occlusion. Methods: The right kidneys of 64 male Sprague Dawley rats were removed to establish an isolated kidney model. The rats were then divided into four treatment groups: Group 1 was the sham treatment group; Group 2, received only low-energy (12 kv, 1 Hz, 200 times) shock wave preconditioning; Group 3 received the same low-energy shock wave preconditioning as Group 2, and then the left renal artery was occluded for 45 minutes; and Group 4 had the left renal artery occluded for 45 minutes. At 24 hours and one-week time points after reperfusion, serum inducible nitric oxide synthase (iNOS), neutrophil gelatinase-associated lipocalin (NGAL), kidney injury molecule-1 (KIM-1), creatinine (Cr), and cystatin C (Cys C) levels were measured, malondialdehyde (MDA) in kidney tissue was detected, and changes in nephric morphology were evaluated by light and electron microscopy. Results: Twenty-four hours after reperfusion, serum iNOS, NGAL, Cr, Cys C, and MDA levels in Group 3 were significantly lower than those in Group 4; light and electron microscopy showed that the renal tissue injury in Group 3 was significantly lighter than that in Group 4. One week after reperfusion, serum NGAL, KIM-1, and Cys C levels in Group 3 were significantly lower than those in Group 4. Conclusion: Low-energy shock wave preconditioning can reduce renal ischemic reperfusion injury caused by renal artery occlusion in an isolated kidney rat model.(AU)

X-ray dynamic observation of cervical degenerative disease induced by unbalanced dynamic and static forces in rats

Purpose: To investigate dynamically the X-ray appearance of cervical degenerative disease induced by unbalanced dynamic and static forces in rats. Methods: A total of 60 Sprague Dawley rats were randomized into test (n=45) and control (n=15) groups, which were randomly subdivided into the one-, three- and six-month post-operative groups. The test group included 10, 15 and 20 rats at the respective corresponding post-operative stage and the control group included five rats at each time-point. By excising cervicodorsal muscles, interspinous ligaments and supraspinous ligament of rats in the test group, the balance of dynamic and static forces on cervical vertebrae was disrupted to establish a rat model of cervical degeneration. Spinal X-ray images were acquired, and intervertebral disc space and intervertebral foramen size were measured at one, three and six months post-operation. The results were analyzed and compared among groups. Results: Cervical dynamic and static imbalance accelerated the appearance of cervical degenerative disease on X-ray. Conclusion: Cervical degenerative disease may be induced by unbalanced dynamic and static forces in rats.(AU)