Journal of physiology and biochemistry (J PHYSIOL BIOCHEM )

Description

  • Impact factor
    1.65
    Show impact factor history
     
    Impact factor
  • 5-year impact
    1.62
  • Cited half-life
    4.00
  • Immediacy index
    0.32
  • Eigenfactor
    0.00
  • Article influence
    0.39
  • Website
    Journal of Physiology & Biochemistry website
  • Other titles
    Journal of physiology and biochemistry (Online)
  • ISSN
    1138-7548
  • OCLC
    70708332
  • Material type
    Document, Periodical, Internet resource
  • Document type
    Internet Resource, Computer File, Journal / Magazine / Newspaper

Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: The flavonoid content of tea (Camellia sinensis) has beneficial properties in the prevention of diseases. However, the mechanisms by which white tea can protect against oxidative stress remain unclear. To shed light on this issue, rats were given distilled water (controls), 0.15 mg/d (dose 1) or 0.45 mg/d (dose 2) of solid tea extract/kg body weight for 12 months. All the animals received an injection of adriamycin (ADR) (10 mg/kg body weight), except half of the control group, which were given an injection of saline solution. The expression of the nuclear factor, E2-related factor 2 (Nrf2), NAD(P)H:quinone oxidoreductase (Nqo1), glutathione–S–transferase (Gst), heme oxygenase-1 (Ho1), catalase (Cat), superoxide dismutase (Sod) and glutathione reductase (Gr) in liver, was analysed by real-time PCR, and the activity of catalase (CAT), superoxide dismutase (SOD) and glutathione reductase (GR) was measured spectrophotometrically. ADR significantly increased the expression of Nrf2, Gst, Nqo1, Ho1, Cat, Sod and Gr with respect to the control levels and also increased the activity of CAT, SOD and GR. The intake of white tea increased in a higher degree the expression of Nrf2, Gst, Nqo1 and Ho1 in the tea + ADR group compared with the control group and C+ ADR group. In addition, tea + ADR groups decreased the expression and activity of CAT, SOD and GR in a dose-dependent manner.
    Journal of physiology and biochemistry 09/2014;
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    ABSTRACT: In vertebrates, chemosensitivity of nutrients occurs through the activation of taste receptors coupled with G-protein subunits, including α-transducin (Gαtran) and α-gustducin (Gαgust). This study was aimed at characterising the cells expressing Gαtran immunoreactivity throughout the mucosa of the sea bass gastrointestinal tract. Gαtran immunoreactive cells were mainly found in the stomach, and a lower number of immunopositive cells were detected in the intestine. Some Gαtran immunoreactive cells in the stomach contained Gαgust immunoreactivity. Gastric Gαtran immunoreactive cells co-expressed ghrelin, obestatin and 5-hydroxytryptamine immunoreactivity. In contrast, Gαtran immunopositive cells did not contain somatostatin, gastrin/cholecystokinin, glucagon-like peptide-1, substance P or calcitonin gene-related peptide immunoreactivity in any investigated segments of the sea bass gastrointestinal tract. Specificity of Gαtran and Gαgust antisera was determined by Western blot analysis, which identified two bands at the theoretical molecular weight of ~45 and ~40 kDa, respectively, in sea bass gut tissue as well as in positive tissue, and by immunoblocking with the respective peptide, which prevented immunostaining. The results of the present study provide a molecular and morphological basis for a role of taste-related molecules in chemosensing in the sea bass gastrointestinal tract.
    Journal of physiology and biochemistry 01/2013;
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    ABSTRACT: Hypoxic preconditioning (PC) was studied using rat atria set up isometrically in 10 mM dextrose medium and paced at 1 Hz, applying three different protocols wherein fed and 24-h fasted rats were used in protocols 1 and 2 and only the fed in protocol 3. In protocol 1, PC was achieved applying a 5 min hypoxia followed by 10 min of reoxygenation before the onset of a 60 min hypoxia and 60 min reoxygenation. In protocol 2 the 5 min and a posterior 45 min hypoxia were applied in the absence of dextrose whereas in the 10 min and 60 min reoxygenation periods dextrose was present. In protocol 3, two cycles of 5 min dextrose-free hypoxic periods were applied before the sustained hypoxia (dextrose-free) and reoxygenation periods (10 min and final 45 min, both in the presence of dextrose). In the control groups of all protocols, the equilibration periods were prolonged to compensate the duration of PC. In the control groups of protocols 1 and 2, the sustained hypoxia evoked greater disturbances of contractility and a smaller post-hypoxic recovery in the fasted than in the fed rat atria. In protocol 1, PC markedly reduced the rise in resting tension and improved the post-hypoxic recovery in the fasted rat atria whereas in the fed rat atria protective effects were small and brief. In protocol 2, PC evoked a small reduction of contracture only in the atria from fasted rats and in protocol 3, PC exacerbated the hypoxic disturbances. These data suggest that PC effects depend both on the severity of the PC stress and the sustained hypoxia; and that PC does not require coronary flow. Se estudia el precondicionamiento hipóxico (PC) en registros isométricos de aurículas de rata montadas isométricamente en medio con glucosa 10 mM y estimuladas a 1 Hz. Se aplican tres protocolos usando ratas alimentadas o en ayunas de 24-h en los 1 y 2, y sólo alimentadas en el 3. En el protocolo 1, el PC consiste en 5 min de hipoxia seguido de 10 min de reoxigenación antes de aplicar 60 min de hipoxia y reoxigenación de 60 min. En el protocolo 2, se aplica 5 min de hipoxia en medio sin sustrato y la hipoxia ulterior de 45 min también en medio sin sustrato, que se repone al reoxigenar durante los períodos de 10 y 60 min. En el protocolo 3, se aplican dos ciclos de 5 min de hipoxia sin sustrato seguidos de 10 min de reoxigenación con sustrato antes de la hipoxia de 45 min sin sustrato y 60 min de reoxigenación con sustrato. En los tres protocolos, la duración del período de equilibrio de los grupos controles se prolonga para compensar la duración del PC. La hipoxia prolongada en los grupos controles de los protocolos 1 y 2 provoca un mayor deterioro de la contractilidad y menor recuperación al reoxigenar en las aurículas de ratas en ayunas. En el protocolo 1, el PC reduce marcadamente la contractura y mejora la recuperación al reoxigenar en las ratas en ayunas mientras que en las alimentadas, todos los efectos beneficiosos son pequeños y efímeros. En el protocolo 2, el PC sólo produce una leve reducción de la contractura en los animales en ayunas y en el protocolo 3, el PC resulta francamente nocivo. Los resultados sugieren que los efectos del PC dependen de la severidad del estímulo precondicionante y de la hipoxia prolongada y que el PC no requiere la circulación coronaria. Key wordsPreconditioning-Hypoxia-Fasting-Rat atria Palabras clavePrecondicionamiento-Hipoxia-Ayuno-Aurícula-Rata
    Journal of physiology and biochemistry 04/2012; 56(4):321-327.
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    ABSTRACT: To investigate the association of matrix metalloproteinase-3 (MMP-3) polymorphism with susceptibility to coronary artery stenosis (CAS) and the number of diseased vessels in patients with type 2 diabetes mellitus (T2DM). The study population comprised 618 unrelated Iranian individual subjects, including 305 angiographically documented CAS patients with T2DM and 313 control subjects with T2DM. MMP3 genotypes were determined by polymerase chain reaction and restriction fragment length polymorphism. Significant differences between cases and controls were observed for MMP3 genotype frequencies (p<0.01). The 6A allele was high frequently seen in the disease group, compared with the control group (64.75 vs. 56.24%, 6A/6A + 5A/6A vs. 5A/5A, p<0.05). The association of this polymorphism with the severity of stenosis were also evaluated which according to results distribution of MMP3 genotypes were not significantly different as compared with the severity of stenosis (p>0.05). Frequency of the 6A allele of the human MMP3 gene is an independent risk factor for CAS in the Iranian T2DM studied.
    Journal of physiology and biochemistry 12/2010; 66(4):359-64.
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    ABSTRACT: Spontaneously hypertensive rat (SHR) offspring from L-arginine- and antioxidant-supplemented SHR dams had persistent lower blood pressure in adulthood. We investigated the influence of vascular mechanism in this effect. We analyzed response to acetylcholine and phenylephrine in aorta and superior mesenteric arteries from Wistar-Kyoto (WKY), SHR, and SHR perinatally supplemented with L-arginine and 4-hydroxy-2,2,6,6-tetramethylpiperidinoxyl (TEMPOL; SHR-suppl). Supplements reduced blood pressure persistently in SHR. Relaxation to acetylcholine was greater in WKY than SHR and remained unmodified in SHR-suppl compared with SHR. Acute TEMPOL did not alter relaxation to acetylcholine in WKY but increased it similarly in SHR and SHR-suppl. Phenylephrine contraction was increased in SHR compared to WKY. In SHR-suppl, this response was similar to SHR. Endothelium removal or N-nitro-L-arginine methyl ester (L-NAME) increased contraction to phenylephrine more in WKY than SHR. In SHR-suppl, this was similar to SHR. In both SHR and SHR-suppl, TEMPOL similarly reduced phenylephrine response. This effect was prevented by L-NAME. Results exposed reinforce the concept that oxidative stress during perinatal period is a contributing factor to the development of hypertension in SHR. Results also reveal that the beneficial effect of this supplementation does not appear to be related to improved endothelial function, suggesting that other regulatory mechanisms of blood pressure may be involved.
    Journal of physiology and biochemistry 12/2010; 66(4):301-9.
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    ABSTRACT: The purpose of the investigation was to observe the pineal-adrenal-immune system relationships and their influence on non-specific immune response in female goats under short-term thermal stress. Six female goats had been exposed to 40°C and 60% relative humidity in the psychrometric chamber for 17 days. Blood samples were obtained on days 0 and 10 to establish control and thermal stress effects, respectively. Chemical adrenalectomy was achieved by injecting metyrapone (100 mg/kg body weight) followed by exogenous melatonin treatment (0.1 mg/kg body weight) from 11th to 17th day of experiment. Thermal stress significantly (P≤0.05) altered the physiological responses. Metyrapone and melatonin treatment significantly (P≤0.05) reduced the thermal-stress-induced increase in plasma concentrations of cortisol and corticosterone while significantly (P≤0.05) increased the plasma melatonin on days 11 and 17. Furthermore, these treatments significantly (P<0.05) increased the phagocytic activity of neutrophils as compared to both control and thermal exposure values from 11-17 days of experiment. The data generated from this study help us to understand the functional relationship between pineal, adrenal, and immune system, and how this relationship modifies the non-specific immune response for the well being of goats during thermal stress.
    Journal of physiology and biochemistry 12/2010; 66(4):339-49.
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    ABSTRACT: Enzymes in mitochondria play an important role in biological oxidation and energy production. To understand the effect of schistosomiasis on these important processes, succinate cytochrome c reductase (SCR) from control and Schistosoma-infected mice was subjected for investigation. In this article, we report that SCR from Schistosoma-infected mouse showed a significant decrease in its Vmax and Km compared to control using both cytochrome c and 2,6-dichlorophenolindophenol as substrates. Furthermore, the kinetic studies of the purified SCR in the absence and presence of the schistosomicidal drugs praziquantel and Commiphora extract reveal that both drugs have an inhibitory action on the enzyme from the control and Schistosoma-infected mice and praziquantel changes the type of inhibition of SCR towards cytochrome c from mixed type in control to a competitive one in the case of the infection.
    Journal of physiology and biochemistry 12/2010; 66(4):291-9.
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    ABSTRACT: Nitric oxide (NO) is a short-lived radical that functions as a neurotransmitter in the central nervous system and plays a physiological role in the regulation of hypothalamic-pituitary-adrenal axis and vasopressinergic axis. In the present study, we aimed to investigate the interaction between the generation of NO and vasopressin (AVP) and corticosterone release after 3 days of water deprivation in rats. Animals were previously treated with intraperitoneal (i.p.) saline or L-nitro-arginine methyl ester (L-NAME) injection. L-NAME is a nonspecific inhibitor of nitric oxide synthases. In control rats given i.p. saline or L-NAME, hypothalamic, pituitary, and plasma AVP levels and plasma corticosterone did not change from baseline levels (p>0.05). Three days of water deprivation increased significantly the corticosterone levels in plasma (p<0.01) and AVP levels in hypothalamus and plasma (p<0.01), but not in pituitary, which showed a significant decrease. These variations were concomitant with the elevation of nitrates/nitrates in plasma. L-NAME injection abolished significantly (p<0.01) the elevation of plasma corticosterone and hypothalamic AVP levels induced by water deprivation. These findings showed that in water-deprived rats, nitric oxide synthase inhibition by L-NAME inhibits corticosterone and vasopressin release, suggesting a potent stimulatory role of NO.
    Journal of physiology and biochemistry 12/2010; 66(4):271-81.
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    ABSTRACT: Vitamin A plays physiological and antioxidants properties and is associated with protective effects on arterial level. However, deleterious effects have been reported, including those observed by our group, which has demonstrated pro-oxidant properties in other systems. Therefore, it is needed to better understand the redox effects of retinoids on arterial system. Thus, our aim was to compare vascular redox parameters among animals supplemented or not with vitamin A. Eighty-five adult male rats were treated with different retinyl palmitate doses (1,000-9,000 IU kg(-1) day(-1)) or saline for 3 (25 rats, n=5 for each group), 7 (25 rats, n=5 for each group), and 28 (35 rats, n=7 for each group) days periods. Aorta artery was surgically removed, cleaned to remove the blood, and homogenized. It was evaluated thiobarbituric reactive species (TBARS), total reduced sulfhydryl (SH), and activities of superoxide dismutase (SOD) and catalase (CAT). Statistics were conducted by one-way ANOVA with Dunnet's post hoc and significance value of p≤0.05. About TBARS, we observed no modifications after 3 days, but a decrease after 7 days in all doses and after 28 days in three higher doses. The two higher doses yielded an increase on SH only after 3 days. SOD activity decreased in three higher doses after 3 days and in all doses after 28 days, but no modifications after 7 days, while CAT activity increased in all doses after 3 days, decreased in all doses after 7 days, and did not change after 28 days. In conclusion, vitamin A induces antioxidant status on vascular level.
    Journal of physiology and biochemistry 12/2010; 66(4):351-7.
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    ABSTRACT: Glutathione (GSH) forms a part of the antioxidant system that plays a vital role in preventing oxidative stress, and an imbalance in the oxidant/antioxidant system has been linked to the pathogenesis of hypertension. The aim of this study was to investigate the status of the GSH system in the kidney of spontaneously hypertensive rats (SHR). Components of the GSH system, including glutathione peroxidase (GPx), glutathione reductase (GR), glutathione-S-transferase (GST), and total GSH content, were measured in the kidneys of 4, 6, 8, 12, and 16 weeks old SHR and Wistar-Kyoto (WKY) rats. Systolic blood pressure of SHR was significantly higher from the age of 6 weeks onwards compared with age-matched WKY rats. GPx activity in the SHR was significantly lower from the age of 8 weeks onwards when compared to that in age-matched WKY rats. No significant differences were evident in the GPx-1 protein abundance, and its relative mRNA levels, GR, GST activity, and total GSH content between SHR and age-matched WKY rats. The lower GPx activity suggests of an impairment of the GSH system in the SHR, which might be due to an abnormality in its protein rather than non-availability of a cofactor. Its role in the development of hypertension in SHR however remains unclear.
    Journal of physiology and biochemistry 12/2010; 66(4):321-7.
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    ABSTRACT: Cardiac hypertrophy is frequently caused by pressure overload (i.e., high blood pressure or hypertension) and can lead to heart failure. The major objective of the present study was to investigate the proteomic changes in response to the development of left ventricular hypertrophy (LVH) induced by abdominal aortic banding (AB) and its prevention by antihypertensive treatment with angiotensin II receptor blocker (ARB) telmisartan. One week after AB and Sham surgery, rats were assigned into three groups: SHAM-control, aortic banding without treatment (AB-Ctrl) and aortic banding with telmisartan treatment (AB-Telmi; 5mg/kg/day for 8 weeks). Echocardiography, hemodynamics, and pathology were performed to assess LVH. Left ventricular myocardium was sampled. The analysis of proteomic proteins from myocardium was performed by two-dimensional gel electrophoresis and MALDI-TOF-MS. In AB-Ctrl, heart rate, systolic arterial blood pressure, diastolic blood pressure, left ventricular end systolic pressure, interventricular septal thickness at diastole, posterior wall thickness in diastole, heart weight (HW) and HW/body weight (BW) were increased, indicating that both hypertension and LVH developed. Telmisartan prevented hypertension and LVH. Concurrently, among numerous proteins, there were 17 that were differentially expressed among hypertrophic hearts, normal hearts, and the hearts where hypertrophic response was suppressed by ARB treatment. Primarily, proteins involved in cell structure, metabolism, stress and signal transduction exhibited up-regulations in LVH, providing cellular and molecular mechanism for hypertrophic development. These changes were prevented or greatly attenuated by telmisartan regimen. Interestingly, antioxidative-related heat shock protein 2 was detected neither in SHAM-Ctrl nor in AB-Ctrl, but in AB-Telmi. LVH is accompanied by series changes of protein expression. Both LVH and proteomic changes can be prevented by blockade of renin-angiotensin system with telmisartan. These protein alterations may constitute mechanistic pathways leading to hypertrophy development and experimental targets for novel therapeutic strategy.
    Journal of physiology and biochemistry 12/2010; 66(4):329-38.
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    ABSTRACT: Sulfite and related chemical such as sulfite salts and sulfur dioxide has been used as a preservative in food and drugs. This molecule has also been generated from the catabolism of sulfur-containing amino acids. Sulfite is a very reactive and potentially toxic molecule and has to be detoxified by the enzyme sulfite oxidase (SOX). The aim of this study was to investigate the effects of ingested sulfite on erythrocyte antioxidant status by measuring glucose-6-phosphate dehydrogenase (G-6-PD), superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) activities and oxidant status by measuring thiobarbituric acid reactive substances (TBARS) in normal and SOX-deficient rats. Rats were assigned to four groups (n = 10 rats/group) as follows; control (C), sulfite (CS), deficient (D), and deficient + sulfite (DS). SOX deficiency was established by feeding rats a low molybdenum diet and adding to their drinking water 200 ppm tungsten (W). Sulfite (25 mg/kg) was administered to the animals via their drinking water. At the end of 6 weeks, Erythrocyte G-6-PD, SOD, and GPx but not CAT activities were found to be significantly increased with and without sulfite treatment in SOX-deficient groups. Sulfite treatment alone was also significantly increased erythrocytes' SOD activity in CS group compared to control. TBARS levels were found to be significantly increased in CS and DS groups and decreased in D group. When SOX-deficient rats treated with sulfite, TBARS level was still higher than other groups. In conclusion, these results suggested that erythrocyte antioxidant capacity, a defense mechanism against the oxidative challenge, increased by endogenous and exogenous sulfite due to its oxidant nature. This increase was also observed in CS and DS groups but it was insufficient to prevent lipid peroxidation.
    Journal of physiology and biochemistry 09/2010; 66(3):205-12.
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    ABSTRACT: The human body is made of some 250 different cell types. From them, only a small subset of cell types is able to produce histamine. They include some neurons, enterochromaffin-like cells, gastrin-containing cells, mast cells, basophils, and monocytes/macrophages, among others. In spite of the reduced number of these histamine-producing cell types, they are involved in very different physiological processes. Their deregulation is related with many highly prevalent, as well as emergent and rare diseases, mainly those described as inflammation-dependent pathologies, including mastocytosis, basophilic leukemia, gastric ulcer, Crohn disease, and other inflammatory bowel diseases. Furthermore, oncogenic transformation switches some non-histamine-producing cells to a histamine producing phenotype. This is the case of melanoma, small cell lung carcinoma, and several types of neuroendocrine tumors. The bioactive compound epigallocatechin-3-gallate (EGCG), a major component of green tea, has been shown to target histamine-producing cells producing great alterations in their behavior, with relevant effects on their proliferative potential, as well as their adhesion, migration, and invasion potentials. In fact, EGCG has been shown to have potent anti-inflammatory, anti-tumoral, and anti-angiogenic effects and to be a potent inhibitor of the histamine-producing enzyme, histidine decarboxylase. Herein, we review the many specific effects of EGCG on concrete molecular targets of histamine-producing cells and discuss the relevance of these data to support the potential therapeutic interest of this compound to treat inflammation-dependent diseases.
    Journal of physiology and biochemistry 09/2010; 66(3):265-70.
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    ABSTRACT: Iron deposits are associated with lipid phenotype in familial hypertriglyceridemias, mainly familial combined hyperlipidemia (FCH) and familial hypertriglyceridemia (FHTG). In turn, diet plays an important role in hypertriglyceridemias although it is not known if dietary patterns are associated with iron concentration in these disorders. The objective was to determine the relationship between diet and iron deposits, measured through serum ferritin concentration, in patients with FCH and FHTG. The study was composed of 140 patients, 107 with FCH and 33 with FHTG. Subjects completed a validated 137-item food frequency questionnaire. Dividing subjects by ferritin tertiles adjusted by sex, there were no significant differences in dietary patterns except in dairy products consumption which was lower in the highest ferritin tertile. Subjects were also divided by triglycerides tertiles adjusted by sex. Those subjects in the highest tertile had lower HDL cholesterol and higher ferritin concentrations. Regarding to dietary parameters, there were significant differences in marine omega three fatty acids and vegetables presenting higher and lower consumption, respectively, those patients in the highest tertile of triglycerides. Moreover, there was not a significant correlation between dietary iron intake and any parameter, both biochemical and dietary, including ferritin concentrations. In conclusion, in patients with primary hypertriglyceridemia, triglycerides are associated with ferritin concentrations but dietary patterns are not related to iron deposits. Our results highly support the concept that the genetic mechanisms driven to hypertriglyceridemia also favor iron overload.
    Journal of physiology and biochemistry 09/2010; 66(3):229-36.

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