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1.
In previous studies, we have shown that cerebral hypoxia results in increased activity of caspase-9, the initiator caspase,
and caspase-3, the executioner of programmed cell death. We have also shown that cerebral hypoxia results in high affinity
Ca2+–ATPase-dependent increase in nuclear Ca2+-influx in the cerebral cortex of newborn piglets. The present study tests the hypothesis that inhibiting nuclear Ca2+-influx by pretreatment with clonidine, an inhibitor of high affinity Ca2+–ATPase, will prevent the hypoxia-induced increase in caspase-9 and caspase-3 activity in the cerebral cortex of newborn piglets.
Thirteen newborn piglets were divided into three groups, normoxic (Nx, n = 4), hypoxic (Hx, n = 4), and hypoxic treated with clonidine (100 mg/kg) (Hx–Cl, n = 5). Anesthetized, ventilated animals were exposed to an FiO2 of 0.21 (Nx) or 0.07 (Hx) for 60 min. Cerebral tissue hypoxia was documented biochemically by determining levels of ATP and
phosphocreatine (PCr). Caspase-9 and -3 activity were determined spectrofluoro-metrically using specific fluorogenic synthetic
substrates. ATP (μmoles/g brain) was 4.6 ± 0.3 in Nx, 1.7±0.4 in Hx (P < 0.05 vs. Nx), and 1.5 ± 0.2 in Hx–Cl (P < 0.05 vs. Nx). PCr (μmoles/g brain) was 3.6 ± 0.4 in Nx, 1.1 ± 0.3 in Hx (P < 0.05 vs. Nx), and 1.0 ± 0.2 in Hx–Cl (P < 0.05 vs. Nx). Caspase-9 activity (nmoles/mg protein/h) was 0.548 ± 0.0642 in Nx and increased to 0.808 ± 0.080 (P < 0.05 vs. Nx and Hx–Cl) in the Hx and 0.562 ± 0.050 in the Hx–Cl group (p = NS vs. Nx). Caspase-3 activity (nmoles/mg protein/h)
was 22.0 ± 1.3 in Nx and 32 ± 6.3 in Hx (P < 0.05 vs. Nx) and 18.8 ± 3.2 in the Hx–Cl group (P < 0.05 vs. Hx). The data demonstrate that clonidine administration prior to hypoxia prevents the hypoxia-induced increase
in the activity of caspase-9 and caspase-3. We conclude that the high afinity Ca2+–ATPase-dependent increased nuclear Ca2+ during hypoxia results in increased caspase-9 and caspase-3 activity. 相似文献
2.
Jerome Honnorat Michele Accominotti Christiane Broussolle Andree-Carole Fleuret Jean-Jacques Vallon Jacques Orgiazzi 《Biological trace element research》1992,32(1-3):311-316
Zinc status was assessed in 53 diabetic patients: 18 insulin-dependent diabetic patients (IDDM), 22 noninsulin-dependent diabetic
patients (NIDDM) treated with oral antidiabetic agents, and 13 insulin-treated, noninsulin-dependent diabetic patients (IRDM).
Plasma zinc concentrations were in the usual range for healthy subjects in these three groups (15.3±0.9 μmol/L). Urinary zinc
excretions were elevated in the IDDM group (18.3±4.1 μmol/24 h;p<0.01 vs normal) and in the NIDDM group (17.5±3.5 μmol/24 h;p<0.01 vs normal), but normal in the IRDM group (11.3±2.4 μmol/24 h). In 14 NIDDM patients treated with transient continuous
sc insulin injections, urinary zinc decreased from 16.5±2.2 μmol/24 h before insulin treatment to 11.5±0.3 μmol/24 h after
insulin treatment without any modification in plasma zinc concentrations. 相似文献
3.
The present study investigates the correlation between the hypoxia-induced phosphorylation of cyclic AMP response element
binding protein and the expression of apoptotic proteins (proapoptotic proteins Bax and Bad and antiapoptotic proteins Bcl-2
and Bcl-xl) during hypoxia in the cerebral cortex of newborn piglets. Piglets were divided into normoxic (Nx) and hypoxic
(Hx, FiO2 = 0.06 for 1 h) groups. Cerebral tissue hypoxia was documented by ATP and phosphocreatine (PCr) levels. Ser133 phosphorylation of cyclic AMP response element binding (CREB) protein was determined by Western blot analysis using a specific
anti-phosphorylated Ser133-CREB protein antibody. The expression of apoptotic proteins was determined by using specific anti-Bax, anti-Bad, anti-Bcl-2
and anti-Bcl-xl antibodies. ATP and PCr values (μmoles/g brain) in Hx were significantly different from Nx (ATP: 4.40 ± 0.39
in Nx vs. 1.19 ± 0.44 in Hx, P < 0.05 vs. Nx; PCr: 3.60 ± 0.40 in Nx vs. 0.70 ± 0.31 in Hx, P < 0.05 vs. Nx). Ser133 phosphorylated CREB protein (OD × mm2) was 74.55 ± 4.75 in Nx and 127.13 ± 19.36 in Hx (P < 0.05 vs. Nx). The expression of proapoptotic proteins Bax and Bad increased and strongly correlated with the increase in
CREB protein phosphorylation (correlation coefficient r = 0.82 and r = 0.85, respectively). The expression of antiapoptotic proteins Bcl-2 and Bcl-xl did not show correlation with CREB protein
phosphorylation. We conclude that cerebral hypoxia results in differential regulation of CREB protein-mediated expression
of proapoptotic and antiapoptotic proteins in the cerebral cortex of newborn piglets. We propose that the increased expression
of proapoptotic vs antiapoptotic genes will lead to an increased potential for apoptotic programmed cell death in the Hx newborn
brain. 相似文献
4.
Tubek S 《Biological trace element research》2006,114(1-3):127-133
Increased or unchanged urinary zinc excretion has been reported in hypertension. In the present article, this observation
was confirmed in a group of 10 untreated hypertensive patients of both sexes that had no diabetes or obesity. The 24-h zinc
excretion was significantly different between the patients: 7.46±3.01 μmol and healthy controls: 5.19±2.19 μmol (p<0.025). After a 1-mo treatment with 4 mg perindopril per day, a decrease of urinary zinc was observed until it reached levels
not significantly different from those of the healthy controls (5.98±2.13 μmol). The decrease was significantly different
from that of the pretreatment values (p<0.05). 相似文献
5.
Kedzierska K Bober J Ciechanowski K Gołembiewska E Kwiatkowska E Noceń I Dołegowska B Dutkiewicz G Chlubek D 《Biological trace element research》2005,107(1):21-32
The aim of the study was to verify the hypothesis if copper could influence the activity of sodium-transporting systems in
erythrocyte membrane that could be related to essential hypertension. The examined group of patients consisted of 15 men with
hypertension. The control group was 11 healthy male volunteers. The Na+/H+ exchanger (NHE) activity in erythrocytes was determined according to Orlov et al. The activity of transporting systems (ATP-Na+/K+; co-Na+/K+/Cl−; ex-Na+/Li+; free Na+ and K+ outflow [Na+, K+-outflow]) was determined according to Garay's method. The concentration of copper in plasma was assessed using atomic absorption
spectrometry. The activity of ATP-Na+/K+ (μmol/L red blood cells [RBCs]/h) in hypertensive patients was 2231.5±657.6 vs 1750.5±291 in the control (p<0.05), the activity of co-Na+/K+/Cl− (μmol/L RBCs/h) in hypertensives was 171.3±77.9 vs 150.7±53.9 in the control (NS). Na+-outflow (μmol/L RBCs/h) in hypertensives was 118.3±51.6 vs 113.3±24.4 in the control (NS). The K+-outflow (μmol/L RBCs/h) in hypertensives was 1361.7±545.4 vs 1035.6±188.3 in the control (NS). The activity of ex-Na+/Li+ (μmol/L RBCs/h) in hypertensive patients was 266.1±76.1 vs 204.1±71.6 in the control (p<0.05). NHE activity (mmol/L RBCs/h) in hypertensives was 9.7±2.96 vs 7.7±1.33 in the control (p<0.05). In hypertensive patients, negative correlation was found between the activity of Na+/K+/Cl− co-transport and plasma copper concentration (R
s=−0.579, p <0.05) and between the activity of ex-Na+/Li+ and plasma copper concentration (R
s=−0.508, p<0.05). Plasma copper concentration significantly influences the activity of sodium transporting systems in erythrocyte membrane.
Copper supplementation could be expected to provide therapeutic benefits for hypertensive patients. 相似文献
6.
Fenning A Harrison G Dwyer D Rose'Meyer R Brown L 《Molecular and cellular biochemistry》2003,251(1-2):51-59
Endurance exercise is widely assumed to improve cardiac function in humans. This project has determined cardiac function
following endurance exercise for 6 (n = 30) or 12 (n = 25) weeks in male Wistar rats (8 weeks old). The exercise protocol
was
30 min/day at 0.8 km/h for 5 days/week with an endurance test on the 6th day by running at 1.2 km/h until exhaustion. Exercise
endurance increased by 318% after 6 weeks and 609% after 12 weeks. Heart weight/kg body weight increased by 10.2% after
6 weeks and 24.1% after 12 weeks. Echocardiography after 12 weeks showed increases in left ventricular internal diameter in
diastole (6.39 ± 0.32 to 7.90 ± 0.17 mm), systolic volume (49 ± 7 to 83 ± 11 μl) and cardiac output (75 ± 3 to 107 ± 8 ml/min)
but not left wall thickness in diastole (1.74 ± 0.07 to 1.80 ± 0.06 mm). Isolated Langendorff hearts from trained rats displayed
decreased left ventricular myocardial stiffness (22 ± 1.1 to 19.1 ± 0.3) and reduced purine efflux during pacing-induced workload
increases. 31P-NMR spectroscopy in isolated hearts from trained rats showed decreased PCr and PCr/ATP ratios with increased
creatine, AMP and ADP concentrations. Thus, this endurance exercise protocol resulted in physiological hypertrophy
while maintaining or improving cardiac function. (Mol Cell Biochem 251: 51–59, 2003) 相似文献
7.
Ravingerová T Matejíková J Neckár J Andelová E Kolár F 《Molecular and cellular biochemistry》2007,297(1-2):111-120
Endogenous cardiac protection against prolonged ischemic insult can be achieved by repeated brief episodes of ischemia (hypoxia)
or by cardiac adaptation to various stresses such as chronic hypoxia. Activation of phosphatidylinositol 3-kinase (PI3K)/Akt
is involved in antiapoptotic effects, however, it is not clear whether it is required for overall heart salvage including
protection against myocardial infarction and arrhythmias. We focussed on the potential common role of PI3K/Akt in anti-infarct
protection, in the experimental settings of long-term adaptation to chronic intermittent hypobaric hypoxia (IHH; 8 h/day,
25–30 exposures, in vivo rats) and acute ischemic preconditioning (IP; Langendorff-perfused hearts). In addition, we explored the role of PI3K/Akt
in susceptibility to ischemic ventricular arrhythmias. In normoxic open-chest rats, PI3K/Akt inhibitor LY294002 (LY; 0.3 mg/kg)
given 5 min before test occlusion/reperfusion (I/R) did not affect infarct size (IS) normalized to the size of area at risk
(AR). In hypoxic rats, LY partially attenuated IS-limiting effect of IHH (IS/AR 59.7 ± 4.1% vs. 51.8 ± 4.4% in the non-treated
rats; p > 0.05) and increased IS/AR to its value in normoxic rats (64.9 ± 5.1%). In the isolated hearts, LY (5 μM) applied 15 min
prior to I/R completely abolished anti-infarct protection by IP (IS/AR 55.0 ± 4.9% vs. 15.2 ± 1.2% in the non-treated hearts
and 42.0 ± 5.5% in the non-preconditioned controls; p < 0.05). In the non-preconditioned hearts, PI3K/Akt inhibition did not modify IS/AR, on the other hand, it markedly suppressed
arrhythmias. In the LY-treated isolated hearts, the total number of ventricular premature beats and the incidence of ventricular
tachycardia (VT) was reduced from 518 ± 71 and 100% in the controls to 155 ± 15 and 12.5%, respectively (p < 0.05). Moreover, bracketing of IP with LY did not reverse antiarrhythmic effect of IP. These results suggest that activation
of PI3K/Akt cascade plays a role in the IS-limiting mechanism in the rat heart, however, it is not involved in the mechanisms
of antiarrhythmic protection. 相似文献
8.
Abdellatif Chakar Ridha Mokni Philip A. Walravens Philippe Chappuis Fanny Bleiberg-Daniel Jean-Louis Mahu Daniel Lemonnier 《Biological trace element research》1993,38(1):97-106
Plasma zinc, copper, and parameters of growth were measured in a group of 116 French preschool children, 2–5 yr-old from low-income
households. Participants were selected on the basis of Z-scores of weight for height (WHZ) and height for age (HAZ). Zinc
and copper concentrations of children with growth impairment (GI), defined by a WHZ and/or HAZ< −1 Z-score, were compared
to those of age, sex, and ethnic origin matched controls (WHZ and HAZ >−1 Z-score). Mean (±SD) plasma zinc concentration was
12.58±1.84 μmol/L in the GI group, and 13.27±1.98 μmol/L in the controls. The difference of the means of paired samples was
0.69±2.34, and by pairedt-test the significance reachedp=0.028. This effect was primarily a result of the weight retarded group (WHZ <−1 Z-score,p<0.009) and to the girls (p<0.05). There were no significant differences in plasma copper concentrations between groups. These results suggest the presence
of marginal zinc deficiency in French preschool children with low weight for height Z-scores. 相似文献
9.
The present study aims to investigate the mechanism of phosphorylation of apoptotic proteins and tests the hypothesis that
the hypoxia-induced increased tyrosine phosphorylation of apoptotic proteins Bcl-2 and Bcl-xl is Ca2+-influx-dependent. Piglets were divided in normoxic (Nx, n = 5), hypoxic (Hx, n = 5) and hypoxic-pretreated with clonidine (Clo + Hx, n = 4) groups. Hypoxic animals were exposed to an FiO2 of 0.06 for 1 h. Clonidine (12.5 μg/kg, IV) was administered to piglets 30 min prior to hypoxia. Hypoxia was confirmed by
ATP and phosphocreatinine (PCr) levels. Cytosol was isolated and separated by 12% SDS–PAGE and probed with tyrosine phosphorylated
(p) -Bax, Bad, Bcl-2 and Bcl-xl antibodies and bands were detected. The ATP levels (μmol/g brain) in the Nx, Hx, Clo + Hx
were 4.3 ± 1.0 (P < 0.05 vs. Hx, Clo-Hx), 0.9 ± 0.8 and 1.5 ± 0.3, respectively. The PCr levels in the Nx, Hx, Clo + Hx were 2.7 ± 0.7 (P < 0.05 vs. Hx, Clo-Hx), 0.9 ± 0.2 and 0.9 ± 0.9, respectively. Ca2+-influx (pmoles/mg protein) was 4.96 ± 0.94 in Nx, 11.11 ± 2.38 in Hx, and 6.23 ± 2.07 in Clo + Hx (P < 0.05 Nx vs. Hx and Hx vs. Clo + Hx). p-Bcl-2 density was 21.1 ± 1.1 Nx, 58.9 ± 9.6 Hx and 29.5 ± 6.4 Clo + Hx (P < 0.05 vs. Hx). p-Bcl-xl density was 29.6 ± 1.5 Nx, 50.6 ± 7.4 Hx and 32.1 ± 0.1 Clo + Hx (P < 0.05 vs. Hx). p-Bax density was 38.6 ± 16.2 Nx, 46.1 ± 5.5 Hx and 41.6 ± 1.9 Clo + Hx groups (P = NS). p-Bad was 66.7 ± 12.8 Nx, 71.2 ± 6.8 Hx and 78.7 ± 22.5 Clo + Hx groups (P = NS). Results showed that clonidine administration prior to hypoxia prevents the hypoxia-induced increased nuclear Ca2+-influx and increased phosphorylation of Bcl-2 and Bcl-xl while phosphorylation of Bad and Bax was not altered. We conclude
that post-translational modification of anti-apoptotic proteins Bcl-2 and Bcl-xl during hypoxia is nuclear Ca2+-influx-dependent. We propose that blockade of nuclear Ca2+-influx that prevents phosphorylation of antiapoptotic proteins may become a neuroprotective strategy. 相似文献
10.
Esposito P Tinelli C Libetta C Gabanti E Rampino T Dal Canton A 《Cell stress & chaperones》2011,16(2):219-224
Autoimmunity to heat shock protein 60 (HSP60) has been related to atherosclerosis. Chlamydia pneumoniae (CP), the most studied infectious agent implicated in promoting atherosclerosis, produces a form of HSP60, which can induce
an autoimmune response, due to high antigenic homology with human HSP60 (hHSP60). In this study, we evaluated the correlations
among anti-hHSP60 antibodies, CP infection, and cardiovascular disease (CVD) in a high-risk population, such as patients undergoing
hemodialysis (HD). Thirty-two patients (67.9 ± 13.9 years; male/female, 23:9) on regular HD were enrolled. Global absolute
cardiovascular risk (GCR) was assessed using the Italian CUORE Project’s risk charts, which evaluate age, gender, smoking
habits, diabetes, systolic blood pressure, and serum cholesterol. The occurrence of cardiovascular events during a 24-month
follow-up was recorded. Seropositivity to CP and the presence of anti-hHSP60 antibodies were tested by specific enzyme-linked
immunosorbent assays. Inflammation was assessed by measurement of C-reactive protein (CRP) serum levels. Fifteen healthy sex
and age-matched (61.9 ± 9.5 years; male/female, 11:4) subjects were the control group. Fifteen of 32 patients resulted seropositive
for CP. CP + patients were older than CP−, while they did not differ for GCR, CRP, and dialytic parameters. CVD incidence
was significantly higher in CP+ (9 CP+ vs 2 CP−, p < 0.05). Cox analysis recognized that the incidence of CVD was independently correlated with seropositivity to CP (HR, 7.59;
p = 0.01; 95% CI = 1.63–35.4). On the other hand, there were no significant differences in anti-hHSP60 levels among CP+, CP−
and healthy subjects: 18.11 μg/mL (14.8–47.8), 31.4 μg/mL (23.2–75.3), and 24.72 μg/mL (17.7–41.1), respectively. Anti-hHSP60
did not correlate to GCR, CRP, and incidence of CVD. In conclusion, our data suggest that anti-hHSP60 autoimmune response
is not related to CP infection and CP-related CVD risk in HD patients. 相似文献
11.
P. O. Vardevanyan A. P. Antonyan G. A. Manukyan A. T. Karapetyan A. K. Shchyolkina O. F. Borisova 《Molecular Biology》2000,34(2):272-276
Isotherms of the EtBr adsorption on native and denatured poly(dA)poly(dT) in the temperature interval 20–70°C were obtained.
The EtBr binding constants and the number of binding sites were determined. The thermodynamic parameters of the EtBr intercalation
complex upon changes of solution temperature 20–48°C were calculated: 1.0·106 M−1≤K≤1.4·106 M−1, free energy ΔG
o=−8.7±0.3 kcal/mol, enthalpy ΔH
o≅0, and entropy ΔS
o=28±0.5 cal/(mol deg). UV melting has shown that the melting temperature (T
m) of EtBr-poly(dA)poly(dT) complexes (μ=0.022,4.16·10−5 M EtBr) increased by 17°C as compared with the ΔT
m of free homopolymer, whereas the half-width of the transition (T
m) is not changed. It was shown for the first time that EtBr forms complexes of two types on single-stranded regions of poly(dA)poly(dT)
denatured at 70°C: strong (K
1=1.7·105 M−1; ΔG
o=−8.10±0.03 kcal/mol) and weak (K
2=2.9·103 M−1; ΔG
o=−6.0±0.3 kcal/mol).The ΔG
o of the strong and weak complexes was independent of the solution ionic strength, 0.0022≤μ≤0.022. A model of EtBr binding
with single-stranded regions of poly(dA)poly(dT) is discussed. 相似文献
12.
We have previously shown that a low-copper (Cu) diet produced alterations in placental Cu transport and fetal Cu stores. Because
Cu deficiency has been associated with lipid deposition in rat dam liver, we hypothesized that a high fat intake, a prevalent
dietary habit in many populations, may worsen fetal Cu status and its closely linked iron (Fe) deposits. Pregnant rats were
fed one of four diets during the second half of gestation: NFNCu: normal fat (7%), normal Cu (6 mg/kg); HFNCu: high fat (21%),
normal Cu; NFLCu: normal fat, low Cu (0.6 mg/kg), and HFLCu: high fat, low Cu. One day before delivery, dams were anesthetized,
and maternal as well as fetal plasma and tissues were obtained. Maternal, fetal, and placental weights were indistinguishable
regardless of the group. Dam plasma Cu and placental Cu were lower in both LCu groups than in the NFNCu or the HFNCu groups.
However, fetal plasma Cu was similar in all treatment groups. Dam and fetal liver Cu stores were reduced in the LCu groups
compared to the NCu groups. This resulted in lower fetal/maternal liver Cu ratios in the NFLCu (1.79 ± 0.14,p < 0.05) and HFLCu (1.59 ± 0.21,p < 0.05) as compared to the NFNCu (4.12 ± 0.44) and the HFNCu (4.15 ± 0.27). Dam liver Fe was higher in the NFNCu than in
HFNCu group (1.10 ± 0.8 vs. 0.89 ± 0.06 μmol/g,p < 0.05); fetal liver Fe from HFNCu and NFLCu dams was lower than that from NFNCu fetuses (NFNCu: 2.42 ± 0.14; HFNCu: 1.92
± 0.15,p < 0.05; NFLCu: 1.81 ± 0.10,p < 0.01). Fetuses of the HFLCu group had a lower heart Fe than the NFNCu group (0.56 ± 0.03 vs. 44.0 ± 3.0 μg/g,p < 0.01). These data indicate that a maternal high-fat diet can potentially aggravate the effects of Cu deficiency by further
altering fetal Cu and Fe tissue stores. 相似文献
13.
Barrett K McGrowder D Brown P Ragoobirsingh D 《Molecular and cellular biochemistry》2006,293(1-2):9-14
This study was designed to understand the cellular mechanisms responsible for defects in the insulin-stimulated signal transduction pathway in a type 2 diabetic animal model. We examined the in vitro PC-1 phosphodiesterase activity and glucose uptake in adipose tissue of streptozotocin (STZ)-induced type 2 diabetic rats. The PC-1 activity was significantly increased in adipose tissue of diabetic rats (0.54 ± 0.08 nmol PNTP hydrolyzed/mg protein/min) compared with controls (0.29 ± 0.05 nmol PNTP hydrolyzed/mg protein/min, p < 0.05). Upon insulin stimulation (100 nM), glucose uptake in the adipose tissue of the controls (4.17 ± 1.28×10−8 μmol/mg/min) was significantly higher than that in the diabetic rats (1.26 ± 0.35×10−8; p < 0.05). These results suggest that elevated PC-1 phosphodiesterase activity and decreased glucose uptake in adipose tissues may be acquired characteristics contributing to the development of type 2 diabetes mellitus. 相似文献
14.
Monica Daniela Doşa Laurentiu-Tony Hangan Eduard Crauciuc Cristina Galeş Mihai Nechifor 《Biological trace element research》2011,142(1):36-46
Research was performed on a group of 30 patients with non-insulin-dependent diabetes mellitus (NIDDM), who never received
antidiabetic medication before, and on a group of 17 healthy adults. The patients were administered treatment with metformin,
1,000 mg/day. Plasmatic and urinary concentration of magnesium have been measured, copper and zinc along with the concentrations
of glucose, HDL, LDL, cholesterol, tryglicerides, HbA1c, and total erythrocyte magnesium, in advance and after 3 months of
treatment. Data showed significant differences in the NIDDM group vs the control group: for plasma magnesium—1.95 ± 0.19 vs
2.20 ± 0.18 mg/dl, p < 0.001; urine magnesium—237.28 ± 34.51 vs 126.25 ± 38.22 mg/24 h, p < 0.001; erythrocyte magnesium—5.09 ± 0.63 vs 6.38 ± 0.75 mg/dl, p < 0.001; plasma zinc—67.56 ± 6.21 vs 98.41 ± 20.47 μg/dl, p < 0.001; urine zinc—1,347.54 ± 158.24 vs 851.65 ± 209.75 μg/24 h, p < 0.001; plasma copper—111.91 ± 20.98 vs 96.33 ± 8.56 μg/dl, p < 0.001; and urine copper—51.70 ± 23.79 vs 36.00 ± 11.70 μg/24 h, p < 0.05. Treatment with metformin for 3 months modified significant erythrocyte magnesium—5.75 ± 0.61 vs 5.09 ± 0.63 mg/dl,
p < 0.001 and urine magnesium—198.27 ± 27.07 vs 237.28 ± 34.51 mg/24 h, p < 0.001, whereas it did not modify significant the plasmatic and urinary concentration of the other cations. The erythrocyte
magnesium concentration was inversely correlated with HbA1c (r = −0.438, p = 0.015). The plasma level of copper was positively correlated with HbA1c (r = 0.517, p < 0.003), tryglicerides (r = 0.534, p < 0.003), and cholesterol (r = 0.440, p < 0.05), and the plasma level of zinc was inversely correlated with glycemia (r = −0.399, p = 0.029). Our data show a significant action of metformin therapy, by increasing the total intraerythrocyte magnesium concentration
and decreasing the urinary magnesium elimination, positively correlated with the decrease of glycemia and HbA1c in NIDDM patients. 相似文献
15.
Adameová A Kuzelová M Andelová E Faberová V Pancza D Svec P Ziegelhöffer A Ravingerová T 《Molecular and cellular biochemistry》2007,295(1-2):129-136
Both, diabetes mellitus (DM) and hypercholesterolemia (HCH) are known as risk factors of ischemic heart disease, however,
the effects of experimental DM, as well as of HCH alone, on ischemia/reperfusion-induced myocardial injury are not unequivocal.
We have previously demonstrated an enhanced resistance to ischemia-induced arrhythmias in rat hearts in the acute phase of
DM. Our objectives were thus to extend our knowledge on how DM in combination with HCH, a model that is relevant to diabetic
patients with altered lipid metabolism, may affect the size of myocardial infarction and susceptibility to arrhythmias. A
combination of streptozotocin (STZ; 80 mg/kg, i.p.) and the fat–cholesterol diet (1% cholesterol, 1% coconut oil; FCHD) was
used as a double-disease model mimicking DM and HCH simultaneosly occurring in humans. Following 5 days after STZ injection
and FCHD leading to increased blood glucose and cholesterol levels, anesthetized open-chest diabetic, diabetic–hypercholesterolemic
(DM–HCH) and age-matched control rats were subjected to 6-min ischemia (occlusion of LAD coronary artery) followed by 10 reperfusion
to test susceptibility to ventricular arrhythmias in the in vivo experiments and to 30-min ischemia and subsequent 2-h reperfusion for the evaluation of the infarct size (IS) in the Langendorff-perfused
hearts. The incidence of the most life-threatening ventricular arrhythmia, ventricular fibrillation, was significantly increased
in the DM–HCH rats as compared with non-diabetic control animals (100% vs. 50%; p<0.05). Likewise, arrhythmia severity score (AS) was significantly higher in the DM–HCH rats than in the controls (4.9±0.2
vs. 3.5±0.5; p<0.05), but was not increased in the diabetic animals (AS 3.7±0.9; p>0.05 vs. controls). Diabetic hearts exhibited a reduced IS (15.1±3.0% of the area at risk vs. 37.6±2.8% in the control hearts;
p<0.05), however, a combination of DM and HCH increased the size of myocardial infarction to that observed in the controls.
In conclusion, HCH abrogates enhanced resistance to ischemia-reperfusion injury in the diabetic rat heart. 相似文献
16.
Metabolic hotspots at land–water interfaces are important in supporting biogeochemical processes. Here we confirm the generality
of land–aquatic interfaces as biogeochemical hot spots by extending this concept to marine beach cast materials. In situ atmospheric
pCO2, from a respiration chamber (10 cm in diameter and 20 cm high) inserted into wrack deposits, was determined using a high-precision
(±1 ppm) non-dispersive infrared gas analyzer (EGM-4, PP-systems) at 1 minute recording intervals. The wrack deposits supported
high metabolic activities, with CO2 fluxes averaging (±SE) 6.62 ± 0.88 μmol C m−2 s−1, compared to median value of 0.98 μmol C m−2 s−1 (mean 2.21 ± 1.25 μmol C m−2 s−1) for bare sand adjacent to deposits. Wrack metabolic rates ranged 40-fold across beaches, from a minimum of 0.57 ± 0.22 μmol
C m−2 s−1 to a maximum of 20.8 ± 5.04 μmol C m−2 s−1, both derived from beaches with deposits dominated by Sargassum. Rates tended to increase significantly (F test, P < 0.05) from the shoreline to reach maximum rates at about 10 m from the shoreline, declining sharply further from the shoreline,
and increased with increasing thickness of the deposits (maximum about 10 cm deep), declining for thicker deposits. Wrack
differing in composition had similar metabolic rates, although deposits consisting of a mixture of seagrass and algae tended
to show somewhat higher rates. Our results show a meter square of wrack deposit supports a metabolic rate equivalent to that
supported by 3 m2 of living seagrass or macroalgal habitat. In wrack, the marine environment provides organic material and moisture and the
land environment provides oxygen to render wrack ecosystems an efficient metabolic reactor. Intense wrack metabolism should
also be conducive to organismal growth by supporting the development of a cryptic, but diverse wrack-based food web. 相似文献
17.
Arteries stimulated by angiotensin II (AII) to contract do not display the expected augmentation of O2 consumption seen with other cardiovascular contractile agonists. We tested the hypothesis that superoxide (O2−) or other reactive oxidant species generated by AII played a role in the paradoxical O2 consumption response in porcine carotid artery, with or without an intact endothelium. Endothelium-denuded arteries were
incubated with either 1 μM diphenylene iodonium (DPI), an inhibitor of NAD(P)H oxidase, 300 u/ml superoxide dismutase (SOD),
a scavenger of O2−, or 20 U/ml catalase, an enzyme which promotes conversion of O2− (scavenged in the form of H2O2) to O2. DPI treatment resulted in the expected increase in O2 consumption upon contractile activation with AII challenge (1.05± 0.23 μmol/g/min; n = 6, p < .01), as did treatment with SOD (0.67± 0.20 μmol/g/min; n = 4, p < .05). Catalase incubation resulted in a burst of O2 generation upon AII challenge (1.30 ± 0.21 μmol/g/min; n = 10, p < .001). In endothelium-intact arteries, O2 consumption was again not augmented with AII challenge; instead, a burst of O2 production was observed (0.66 ± 0.22 μmol/g/min; n = 9, p < .05), which was not affected further by addition of catalase. Thus, the absence of apparent augmentation of O2 consumption during contractile activation of endothelium-denuded arteries was attributed to simultaneous NAD(P)H oxidase-dependent
production of O2−, and attendant H2O2 and O2 generation which either and masked the detection of O2 consumed or suppressed mitochondrial uptake of O2, or both. An intact endothelium was required to manifest the burst of O2 generation with AII stimulation under normal conditions. (Mol Cell Biochem xxx: 235–239, 2005) 相似文献
18.
The effect of time of day and exercise on platelet functions and platelet–neutrophil aggregates in healthy male subjects 总被引:2,自引:0,他引:2
Platelet activation state changes by exercise. The effect of exercise time on platelet activation state and formation of platelet–neutrophil
aggregates are not known yet. In this study the effect of exercise and time of day were examined on platelet activity with
platelet–neutrophil aggregates. Ten moderately active males aged 27± 1.63 (mean±S.D.) years completed sub-maximal (70% VO2max) exercise trials for 30 min. Blood pressure (BP) was recorded. Venous blood samples were obtained at rest, immediately post-exercise
and after 30 min of recovery. Whole blood was analysed for haematocrit (Hct), haemoglobin (Hb), platelet count (PC), mean
platelet count (MPV) and platelet aggregation (PA). Platelet–neutrophil aggregates and beta-thromboglobulin (β-TG) levels
were assayed. Platelet count showed significant increase after morning exercise ((236± 32)×109 l−1 versus (202± 34)×109 l−1 baseline, p < 0.05). Exercise resulted in significantly lower MPV after the evening exercise (9.16± 0.5 fl versus 9.65± 0.36 fl, p < 0.05). Platelet aggregation by adenosine diphosphate (ADP) decreased after morning exercise and the recovery aggregation
levels were significantly different at two different times of the day (68± 20% a.m. versus 80± 12% p.m., p < 0.05). It was also showed that platelet–neutrophil aggregates increased significantly from baseline after both exercises.
Exercise-induced platelet–neutrophil aggregates were higher in the evening (10.7± 1.3% p.m. versus 6.4± 1.8% a.m., p < 0.0001). It is therefore concluded that besides platelet–platelet aggregation, exercise can cause platelet– neutrophil
aggregates. In addition, time of day has an effect on platelet activation related events. Circadian variations of physiological
parameters may have an effect on thrombus formation by platelet activation. (Mol Cell Biochem xxx: 119–124, 2005) 相似文献
19.
Feridun Kosar Ibrahim Sahin Nusret Acikgöz Yuksek Aksoy Zehra Kucukbay Sengul Cehreli 《Biological trace element research》2005,107(1):1-9
It is known that certain trace elements can affect various heart diseases. In this study, we aimed to evaluate the changes
in concentrations of certain serum trace elements in patients with chronic rheumatic heart disease (RHD). Serum analysis of
selenium (Se), zinc (Zn), and copper (Cu) trace elements was assayed by atomic absorption spectrophotometry. RHD patients
had significantly lower serum concentrations of Se and Zn than control subjects (p<0.05 and p<0.001, respectively). However, the serum Cu concentration was significantly higher in RHD patients than in controls (1.93±0.59
μg/L vs 1.06±0.29 μg/L; p<0.001). Similarly, the Cu/Zn ratio in RHD patients was higher than in control subjects (4.70±0.92 vs 1.68±0.45; p<0.001). Additionally, no significant correlation was found among these trace element concentrations and the functional capacity
classes (p>0.05). RHD patients had decreased serum Se and Zn element concentrations and increased serum Cu element concentration. We
suggest that Se and Zn deficiency might be contributory factors in the development of rheumatic heart disease, and a high
Cu concentration and a high Cu/Zn ratio might reflect an ongoing inflammatory process in this disease. 相似文献
20.
Kimotsuki T Niwa N Hicks MN Dunne M Cobbe SM Watanabe MA 《Journal of biological physics》2010,36(3):299-315
Roughly speaking, restitution is the dependence of recovery time of cardiac electrical activity on heart rate. Increased restitution
slope is theorized to be predictive of sudden death after heart injury such as from coronary artery occlusion (ischemia).
Adrenaline analogs are known to increase restitution slope in normal hearts, but their effects in failing hearts are unknown.
Twenty-six rabbits underwent coronary ligation (n = 15) or sham surgery (n = 11) and implantation of a lead in the heart for recording electrocardiograms. Eight weeks later, unanesthetized rabbits
were given 0.25–2.0 ml of 1 μmol/L isoprenaline intravenously, which increased heart rate. Heart rate was quantified by time
between QRS peaks (RR) and heart activity duration by R to T peak time (QTp). Ligated rabbits (n = 6) had lower ejection fraction than sham rabbits (n = 7, p < 0.0001) indicative of heart failure, but similar baseline RR (269 ± 15 vs 292 ± 23 ms, p = 0.07), QTp (104 ± 17 vs 91 ± 9 ms, p = 0.1), and isoprenaline-induced minimum RR (204 ± 11 vs 208 ± 6 ms, p = 0.4). The trajectory of QTp vs TQ plots displayed hysteresis and regions of negative slope. The slope of the positive slope
region was >1 in ligated rabbits (1.27 ± 0.66) and <1 in sham rabbits (0.35 ± 0.14, p = 0.004). The absolute value of the negative slope was greater in ligated rabbits (− 0.81 ± 0.52 vs − 0.35 ± 0.14, p = 0.04). Isoprenaline increased heart rate and slopes of restitution trajectory in failing hearts. The dynamics of restitution
trajectory may hold clues for sudden death in heart failure patients. 相似文献