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1.
Increased vulnerability of brain to estrogen withdrawal-induced mitochondrial dysfunction with aging
In the present study, to determine whether aging could increase the vulnerability of the brain to estrogen withdrawal-induced
mitochondrial dysfunction, we measured the cytochrome c oxidase (COX) activity and mitochondrial adenosine triphosphate (ATP)
content in hippocampi of 2 groups of ovariectomized (OVX) Wistar rats aged 2 months (young) and 9 months (middle-aged), respectively.
In addition, effects of genistein and estradiol benzoate (EB) were tested also. We observed only a transient alteration of
COX activity and mitochondrial ATP content in hippocampi of young OVX rats but a prolonged lowering of COX activity and mitochondrial
ATP content in hippocampi of middle-aged OVX rats. This suggested that with aging compensatory mechanisms of mitochondrial
function were attenuated, thus exacerbated estrogen withdrawal-induced mitochondrial dysfunction in hippocampi. Significantly,
EB/genistein treatment reversed this estrogen withdrawal-induced mitochondrial dysfunction in both young and middle-aged rats
suggesting that genistein may be used as a substitute for estradiol to prevent age-related disease such as Alzheimer’s disease
in post-menopausal females. 相似文献
2.
In the present study, ovariectomized Sprague-Dawley rats were used to mimic the pathological changes of post-menopausal females with genistein and estradiol benzoate (EB) as substitutes for endogenous estradiol. Measurements of hippocampal ATP content, mitochondrial ATP content and the rate of mitochondrial ATP synthesis in the hippocampus indicated that after ovariectomy, brain energy metabolism of the rats presented a transient change in hippocampal ATP content which was significant from the 6th to the 8th day after ovariectomy. The change on the 6th day was the most noteworthy. Mitochondrial ATP content and the rate of mitochondrial ATP synthesis of the hippocampus were also lowered. However, after using EB or genistein, the three indicators returned to normal. It is suggested that mitochondrial dysfunction may play a key role in Alzheimer's disease (AD) of the post-menopausal female, and may serve as the target for endogenous estrogen and exogenous phytoestrogen. In addition, genistein, which possesses the properties of estrogen but not its side effects such as carcinogenicity, could reverse the bioenergetic defects of ovariectomized rats and perhaps be used as a substitute for estradiol to prevent or treat central neurodegeneration in post-menopausal women. 相似文献
3.
Magali Cros Caroline Silve Anne-Marie Graulet Caroline Morieux Pablo Ureña Marie-Christine de Vernejoul Zhor Bouizar 《Journal of cellular biochemistry》1998,70(1):84-93
The aim of the present study was to test the hypothesis that the decreased renal tubular reabsorption of calcium observed in estrogen deficiency is associated with a local regulation of either PTHrP or PTH/PTHrP receptor genes in the kidney. Rats were randomly sham-operated (S) or ovariectomized receiving either vehicule (OVX) or 4 μg E2/kg/day (OVX+E4) or 40 μg E2/kg/d (OVX+E40) during 14 days using alzet minipumps. Plasma PTH and calcium levels were lower in untreated OVX animals than in all other groups (P < 0.01). Plasma PTH was higher in OVX+E40 than in OVX+E4 (P < 0.05). PTHrP mRNA expression in the kidney was unaffected by ovariectomy but was increased in OVX+E40 (0.984 ± 0.452 for PTHrP/GAPDH mRNAs expression vs. 0.213 ± 0.078 in sham, P < 0.01). PTH/PTHrP receptor mRNA expression and the cAMP response of renal membranes to PTH were unaffected by ovariectomy and estrogen substitution. In conclusion, renal PTHrP and PTH/PTHrP receptor mRNAs are not modified by ovariectomy. However, 17β-estradiol increases renal expression of PTHrP mRNA without evident changes in its receptor expression and function. This may help to explain the pharmacological action of estrogen in the kidney, especially how it prevents the renal leak of calcium in postmenopausal women. J. Cell. Biochem. 70:84–93, 1998. © 1998 Wiley-Liss, Inc. 相似文献
4.
M. Marchlewicz I. Baranowska-Bosiacka A. Kolasa A. Kondarewicz D. Chlubek B. Wiszniewska 《Biometals》2009,22(6):877-887
Adult male Wistar rats were intoxicated with 1% lead acetate (PbAc) administered in drinking water for nine months, which
amounts to a period five times longer than the duration of one spermatogenesis. There were mitochondrial ultrastructure disorders
of epididymal epithelial cells observed in PbAc-treated rats; also a significant lead-induced decrease in ATP concentration
in epididymal epithelial cells (by 32%, P < 0.05), Adenylate Energy Charge value (AEC) (by 8%, P < 0.05) and an increase in ADP (28.5%, P < 0.05), AMP (27%, P < 0.05) and adenosine (by 56%, P < 0.05). The results were measured using high performance liquid chromatography (HPLC) and detected even at low lead concentrations
in whole blood (M:7.03 μg/dL; Q1–Q3: 2.99–7.65). The function of mitochondria in cultured epididymal epithelial cells of control
and PbAc-treated animals were evaluated using fluorophores: Mitotracker Green FM and JC-1. After incubation with Mitotracker
Green FM, we observed active mitochondria producing bright green fluorescence in the cytoplasm of cultured epididymal epithelial
cells, both in the control group and the Pb-treated animals. Incubation of cultured epididymal epithelial cells of animals
from both groups produced red-orange fluorescence with the mitochondrial JC-1 probe indicating mitochondria with high membrane
potential (ΔΨm > 80–100 mV) and green fluorescence in the mitochondria with low membrane potential (ΔΨm <80 mV). The results
showed that a chronic low-level exposure to lead, even without severe clinical symptoms of contamination, disrupted the ultrastructure
and energy metabolism of mitochondria in epididymal epithelial cells. 相似文献
5.
6.
Fei Xu Guobin Wang Kailin Cai Ronglin Zhai Shouyuan Tang 《Molecular biology reports》2010,37(3):1397-1401
To study the effects of ovariectomy on tumorigenesis and microsatellite instability (MSI) in rat colon tumors induced by 1,2-dimethylhydrazine,
to elucidate the association between postmenopausal ovarian hormones depletion and MSI pathway in colorectal tumorigenesis.
Forty female Wistar rats were randomly divided into two groups: Ovariectomized (Ovx) group and Sham-ovariectomized (Sham-Ovx)
group. All rats were injected intraperitoneally with 1,2-dimethylhydrazine (DMH) (20 mg/kg b.w) once a week for 20 weeks.
Ten weeks after the final DMH injection, all the rats were sacrificed to collect tumors. Microsatellite instability of six
microsatellite loci was detected using fluorescent PCR followed by fragment analysis on automatic DNA sequencer with GeneScan
3.7 software. The tumor multiplicity in the OVX group was significantly higher than that in the Sham-OVX group (3.6 ± 1.4
vs. 2.4 ± 1.6, P < 0.05). The incidence of MSI-positive tumors in OVX group was higher than that in Sham-OVX group (32.1 vs. 10.8%, P < 0.05).The incidence of tumors showing MSI at multiple loci in OVX group was also higher than that in Sham-OVX group (18.9
vs. 2.7%, P < 0.05). Ovariectomy increased tumor formation and the frequency of MSI in DMH-induced colon tumors. It implied that postmenopausal
ovarian hormones depletion might influence colorectal tumorigenesis through MSI pathway. 相似文献
7.
He F Tai F Zhang Y Zhang X 《Journal of comparative physiology. A, Neuroethology, sensory, neural, and behavioral physiology》2012,198(5):347-362
Aggression in socially monogamous mandarin vole (Microtus mandarinus) was observed after castration. Levels of serum sex hormones and their central receptors were also measured using enzyme-linked
immunosorbent assay and immunohistochemistry methods. The data indicate that adult males showed higher levels of aggression
after castration. However, castration significantly reduced levels of serum testosterone, and the number of androgen receptor
immunoreactive neurons in the anterior hypothalamus, bed nucleus of the stria terminalis, medial amygdaloid nucleus (P < 0.01) and lateral septal nucleus (P < 0.05). In addition, levels of estrogen receptor β in the anterior hypothalamus and medial amygdaloid nucleus (P < 0.05), bed nucleus of the stria terminalis and lateral septal nucleus (P < 0.01) declined to varying degrees at weekly intervals. In contrast, serum 17β-estradiol concentrations were up-regulated
by castration and castration did not change levels of estrogen receptor α in the medial amygdaloid nucleus and lateral septal
nucleus, but increased it in the anterior hypothalamus 3 weeks after castration (P < 0.05). We suggest that higher levels of aggression induced by castration may be independent of serum testosterone and androgen
receptors, and may be associated with high serum 17β-estradiol concentrations, stable estrogen receptor α immunoreactive neurons
in some brain regions and the relative ratio of the two estrogen receptors. 相似文献
8.
9.
Partial attenuation of cytotoxicity and apoptosis by SOD1 in ischemic renal epithelial cells 总被引:1,自引:0,他引:1
Huan Ling Liang Jody Arsenault Jordan Mortensen Frank Park Christopher P. Johnson Vani Nilakantan 《Apoptosis : an international journal on programmed cell death》2009,14(10):1176-1189
Reactive oxygen species (ROS) contribute significantly to apoptosis in renal ischemia-reperfusion (IR) injury, however the
exact mechanisms are not well understood. We used novel lentiviral vectors to over-express superoxide dismutase 1 (SOD1) in
proximal tubular epithelial (LLC-PK1) cells and determined effects of SOD1 following ATP depletion-recovery, used as a model to simulate renal IR. SOD1 over-expression
partially protected against cytotoxicity (P < 0.001) and decreased superoxide (O2
•−) in ATP depleted cells. The ATP depletion-mediated increase in nuclear fragmentation, an index of apoptosis and activation
of caspase-3 was also partially blocked by SOD1 (P < 0.05). However, SOD1 over-expression was insufficient to completely attenuate caspase-3, indicating that ROS other than
cytoplasmic O2
•− are involved in ATP depletion mediated injury. To test the contribution of hydrogen peroxide, a subset of enhanced green
fluorescent protein (EGFP) and SOD1 (serum free and injured) cells were treated with polyethylene glycol-catalase (PEG-catalase).
As expected there was 50% reduction in cytotoxicity and caspase-3 in SOD1 cells compared to EGFP cells; catalase treatment
decreased both indices by an additional 28% following ATP depletion. To test the role of mitochondrial derived superoxide,
we also treated a subset of LLC-PK1 cells with the mitochondrial antioxidant, MitoTEMPO. Treatment with MitoTEMPO also decreased ATP depletion induced cytotoxicity
in LLC-PK1 cells in a dose dependant manner. These studies indicate that both SOD1 dependent and independent pathways are integral in
protection against ATP depletion-recovery mediated cytotoxicity and apoptosis, however more studies are needed to delineate
the signaling mechanisms involved. 相似文献
10.
This study was undertaken to evaluate theeffects of regular endurance-type exercise on glucose tolerance andglucose-stimulated insulin response (GSIR) in ovariectomized (OVX) ratswith and without estrogen replacement. To do that, OVX Sprague-Dawleyrats were compared with an OVX estradiol-treated group (OVXE2) and asham-operated (Sham) group. Each of these groups was subdivided into asedentary and a treadmill-trained (8 wk) group. Intravenous glucosetolerance tests (0.5 g/kg) were conducted in all rats 48 h afterthe last training session. Plasma levels of 17-estradiol and theuterus weight were significantly (P < 0.05) lower inOVX compared with results in Sham and significantly (P < 0.01) higher in OVXE2 (hyperestrogenic) compared with results inSham. Body weights were significantly (P < 0.01)different among groups, in the following decreasing order: OVX, Sham,and OVXE2. The average daily food intake was significantly(P < 0.01) increased in OVX rats compared with Sham,whereas estradiol treatment diminished this effect (P < 0.01). Exercise training was found to alter none of theabove-mentioned variables in all three experimental conditions. Although the mean integrated area under the glucose and insulin curveswas not affected by OVX, training induced a significant (P < 0.01) reduction in the mean integrated area underthe insulin curve in all three experimental conditions. It is concludedthat the positive effects of physical training on improving GSIR in OVXand hyperestrogenic animals are similar to what has been found in Sham. 相似文献
11.
12.
Høegh-Andersen P Tankó LB Andersen TL Lundberg CV Mo JA Heegaard AM Delaissé JM Christgau S 《Arthritis research & therapy》2004,6(2):R169-R180
We aimed to assess the effect of ovariectomy on cartilage turnover and degradation, to evaluate whether ovariectomized (OVX)
rats could form an experimental model of postmenopausal osteoarthritis. The effect of ovariectomy on cartilage was studied
using two cohorts of female Sprague–Dawley rats, aged 5 and 7 months. In a third cohort, the effect of exogenous estrogen
and a selective estrogen receptor modulator was analyzed. Knee joints were assessed by histological analysis of the articular
cartilage after 9 weeks. Cartilage turnover was measured in urine by an immunoassay specific for collagen type II degradation
products (CTX-II), and bone resorption was quantified in serum using an assay for bone collagen type I fragments (CTX-I).
Surface erosion in the cartilage of the knee was more severe in OVX rats than in sham-operated animals, particularly in the
7-month-old cohort (P = 0.008). Ovariectomy also significant increased CTX-I and CTX-II. Both the absolute levels of CTX-II and the relative changes
from baseline seen at week 4 correlated strongly with the severity of cartilage surface erosion at termination (r = 0.74, P < 0.01). Both estrogen and the selective estrogen receptor modulator inhibited the ovariectomy-induced acceleration of cartilage
and bone turnover and significantly suppressed cartilage degradation and erosion seen in vehicle-treated OVX rats. The study
indicates that estrogen deficiency accelerates cartilage turnover and increases cartilage surface erosion. OVX rats provide
a useful experimental model for the evaluation of the chondroprotective effects of estrogens and estrogen-like substances
and the model may be an in vivo representation of osteoarthritis in postmenopausal women. 相似文献
13.
Ferreira MC Cavallo IK Florio P Petraglia F Reis FM 《Journal of molecular histology》2008,39(5):535-541
Activin A is a growth factor expressed in the endometrium, where it modulates tissue remodeling and enhances decidualization.
The effects of activin A are counteracted by two binding proteins, namely follistatin and follistatin-like 3 (FSTL3). We have
evaluated the effects of estrogen and progestin on the endometrial expression of activin βA subunit, follistatin and FSTL3
in ovariectomized rats. Adult female Wistar rats (n = 21) were ovariectomized and received one week later a single dose of estradiol benzoate (1.5 mg/kg body weight, i.m. injection),
either alone (n = 7) or associated with depot medroxyprogesterone acetate (3 mg/kg body weight, i.m. injection, n = 7), or oil vehicle (control group, n = 7). One week later, activin βA subunit mRNA levels had increased significantly in the uteri of rats treated with estradiol
alone (7.4 fold increase over controls, P < 0.05) and to the same extent in rats receiving estradiol plus medroxyprogesterone (6.1 fold increase over controls, P < 0.05). This was accompanied by increase of βA subunit immunostaining in estradiol and estroprogestin treated rats, which
was noted only in the surface endometrial epithelium. Follistatin mRNA expression, conversely, showed a significant decrease
in the groups treated with estrogen alone and estrogen plus progestin (P < 0.05), and follistatin immunostaining in the glandular epithelium was weaker in estradiol and estroprogestin-treated rats
compared to controls. FSTL3 expression was similar in the 3 groups. In conclusion, the expression of activin βA subunit increases
and that of follistatin decreases following estrogen replacement in the endometrium of ovariectomized rats, and these effects
are not further altered by the addition of progestin.
Presented, in part, as a poster at the 55nd Annual Meeting of the Society for Gynecologic Investigation, San Diego, CA, March
2008. 相似文献
14.
Mythri RB Venkateshappa C Harish G Mahadevan A Muthane UB Yasha TC Srinivas Bharath MM Shankar SK 《Neurochemical research》2011,36(8):1452-1463
Dopaminergic neurons die in Parkinson’s disease (PD) due to oxidative stress and mitochondrial dysfunction in the substantia
nigra (SN). We evaluated if oxidative stress occurs in other brain regions like the caudate nucleus (CD), putamen (Put) and
frontal cortex (FC) in human postmortem PD brains (n = 6). While protein oxidation was elevated only in CD (P < 0.05), lipid peroxidation was increased only in FC (P < 0.05) and protein nitration was unchanged in PD compared to controls. Interestingly, mitochondrial complex I (CI) activity
was unaffected in PD compared to controls. There was a 3–5 fold increase in the total glutathione (GSH) levels in the three
regions (P < 0.01 in FC and CD; P < 0.05 in Put) but activities of antioxidant enzymes catalase, superoxide dismutase, glutathione reductase and glutathione-s-tranferase
were not increased. Total GSH levels were elevated in these areas because of decreased activity of gamma glutamyl transpeptidase
(γ-GT) (P < 0.05) activity suggesting a decreased breakdown of GSH. There was an increase in expression of glial fibrillary acidic
protein (GFAP) (P < 0.001 in FC; P < 0.05 in CD) and glutathione peroxidase (P < 0.05 in CD and Put) activity due to proliferation of astrocytes. We suggest that increased GSH and astrocytic proliferation
protects non-SN brain regions from oxidative and mitochondrial damage in PD. 相似文献
15.
E-Jian Lee Yu-Chang Hung Hung-Yi Chen Tian-Shung Wu Tsung-Ying Chen 《Neurochemical research》2009,34(6):1157-1166
We examined whether a nitric oxide scavenger, 2-(4-carboxyphenyl)-4,4,5,5-tetramethyl-imidazoline-l-oxyl-3-oxide (carboxy-PTIO), could offer neuroprotective actions and improve cerebral energy metabolism in a model of stroke.
Sixty C57BL/10J mice were given either carboxy-PTIO (0.3–1.2 mg/kg) or vehicle intraperitoneally, 0.5 h after permanent middle
cerebral artery occlusion, to evaluate the dose–response effects. An additional 70 animals received carboxy-PTIO (0.6 mg/kg)
or vehicle, 2–6 h post-ischemia, for establishing the therapeutic window. Subgroups of animals, treated with carboxy-PTIO
(0.6 mg/kg) or vehicle, were used for measuring cerebral bioenergetic metabolites (ATP, ADP, AMP, adenosine). Mice treated
with carboxy-PTIO (0.6 mg/kg) had dose-specifically reduced brain infarction, significantly by 27–30% (P < 0.05), even when therapy was delayed up to 4 h after the ischemic insult (P < 0.05). Four hour post-ischemia, ATP depleted in the ischemic hemisphere (P < 0.05). Administration with carboxy-PTIO not only improved the recovery of ATP in the ischemic hemisphere (P < 0.05), but also enhanced adenosine content across the ischemic and non-ischemic hemispheres (P < 0.05). The neuroprotection of carboxy-PTIO may be partly attributed to the beneficial effects of improving cerebral energy
metabolism. 相似文献
16.
Shi D Guo S Liao S Su R Guo M Liu N Li P Tang Z 《Biological trace element research》2012,145(3):312-317
To investigate the protection of selenium on hepatic mitochondrial functions, 90 7-day-old ducklings were randomly divided
into three groups (groups I–III). Group I was used as a blank control. Group II was administered with aflatoxin B1 (0.1 mg/kg body weight). Group III was administered with aflatoxin B1 (0.1 mg/kg body weight) plus selenium (sodium selenite, 1 mg/kg body weight). All treatments were given once daily for 21 days.
The results showed that the activities of hepatic mitochondrial complexes I–IV in group II ducklings significantly decreased
when compared with group I (P < 0.01). Furthermore, the activities of hepatic mitochondrial complexes I–IV in group III significantly increased when compared
with group II (P < 0.05). The hepatic mitochondrial respiratory control ratio (RCR) in group II ducklings significantly decreased when compared
with group I (P < 0.01). In addition, the hepatic mitochondrial RCR in group III significantly increased when compared with group II (P < 0.05). These results revealed that the aflatoxin B1 significantly induced hepatic mitochondrial dysfunction in the activities of hepatic mitochondrial respiratory chain complexes
I–IV and the RCR in ducklings. However, sodium selenite could significantly ameliorate the negative effect induced by aflatoxin
B1. 相似文献
17.
Mariona Guitart‐Mampel Diana L. Juarez‐Flores Lina Youssef Constanza Moren Laura Garcia‐Otero Vicente Roca‐Agujetas Marc Catalan‐Garcia Ingrid Gonzalez‐Casacuberta Ester Tobias Jos C. Milisenda Josep M. Grau Ftima Crispi Eduard Gratacos Francesc Cardellach Glria Garrabou 《Journal of cellular and molecular medicine》2019,23(6):3962-3973
Intrauterine growth restriction (IUGR) is an obstetric complication characterised by placental insufficiency and secondary cardiovascular remodelling that can lead to cardiomyopathy in adulthood. Despite its aetiology and potential therapeutics are poorly understood, bioenergetic deficits have been demonstrated in adverse foetal and cardiac development. We aimed to evaluate the role of mitochondria in human pregnancies with IUGR. In a single‐site, cross‐sectional and observational study, we included placenta and maternal peripheral and neonatal cord blood mononuclear cells (PBMC and CBMC) from 14 IUGR and 22 control pregnancies. The following mitochondrial measurements were assessed: enzymatic activities of mitochondrial respiratory chain (MRC) complexes I, II, IV, I + III and II + III, oxygen consumption (cell and complex I‐stimulated respiration), mitochondrial content (citrate synthase [CS] activity and mitochondrial DNA copy number), total ATP levels and lipid peroxidation. Sirtuin3 expression was evaluated as a potential regulator of bioenergetic imbalance. Intrauterine growth restriction placental tissue showed a significant decrease of MRC CI enzymatic activity (P < 0.05) and CI‐stimulated oxygen consumption (P < 0.05) accompanied by a significant increase of Sirtuin3/β‐actin protein levels (P < 0.05). Maternal PBMC and neonatal CBMC from IUGR patients presented a not significant decrease in oxygen consumption (cell and CI‐stimulated respiration) and MRC enzymatic activities (CII and CIV). Moreover, CS activity was significantly reduced in IUGR new‐borns (P < 0.05). Total ATP levels and lipid peroxidation were preserved in all the studied tissues. Altered mitochondrial function of IUGR is especially present at placental and neonatal level, conveying potential targets to modulate obstetric outcome through dietary interventions aimed to regulate Sirtuin3 function. 相似文献
18.
Mitsuhiro Daisu Toshihisa Hatta Yasuko Sakurai-Yamashita Toru Nabika Kouzo Moritake 《Cellular and molecular neurobiology》2009,29(4):557-562
Transient forebrain ischemia and reperfusion induces delayed neuronal death (DND) in the hippocampal Cornu Ammonis 1 (CA1)
subfield of stroke-prone spontaneously hypertensive rat (SHRSP). The vulnerability to DND is potentially related to the genetic
susceptibility to stroke in this strain. To elucidate the mechanism of DND in SHRSP, however, it is essential to establish
a method for quantitative evaluation of DND, which is not available yet. Male SHRSPs and spontaneously hypertensive rats (SHRs)
at 12 weeks of age were used in the experiment. The bilateral common carotid arteries were surgically occluded with aneurysmal
clips for 10 min. The brain was taken out 7 days after the experiment of the transient ischemia, and was sliced into serial
coronal sections. Quantitative estimation of the number of viable pyramidal cells in the CA1 and CA2/3 subfields was performed
based on the stereology with a random and systematic sampling. The transient ischemia and reperfusion (TIR) significantly
reduced the number of viable pyramidal cells in CA1 of SHRSP (61000 ± 20100 in TIR vs. 128500 ± 21900 in the sham-operation, P < 0.000001 by Student’s t-test), while no significant difference was observed in SHR (140300 ± 30800 in TIR vs. 128200 ± 16700 in the sham-operation,
P = 0.35). Further analysis revealed a dorsal-ventral gradient in the distribution of DND in CA1 of SHRSP with the most severe
change in the dorsal area. The quantitative measurement using a stereological method is useful in the precise evaluation of
DND in SHRSP. This method can be applied in the studies of effects of medical treatments on the ‘ischemia/reperfusion’ insult. 相似文献
19.
The aim of the study was to investigate the effect of selenium on hepatic mitochondrial antioxidant capacity in ducklings
administrated with aflatoxin B1 (AFB1). Ninety 7-day-old ducklings were randomly divided into three groups (groups I–III). Group I was used as a blank control.
Group II was administered with AFB1 (0.1 mg/kg body weight). Group III was administered with AFB1 (0.1 mg/kg body weight) plus selenium (sodium selenite, 1 mg/kg body weight). All treatments were given once daily for 21 days.
The results showed that the activities of mitochondrial superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase
(GSH-Px), and glutathione reductase (GR) in group II ducklings significantly decreased when compared with group I (P < 0.01). Furthermore, the content of hepatic mitochondrial malondialdehyde (MDA) significantly increased (P < 0.01). However, the activities of hepatic mitochondrial SOD, CAT, GSH-Px, and GR in group III ducklings significantly increased
when compared with group II (P < 0.05). In addition, the content of hepatic mitochondrial MDA significantly decreased (P < 0.01). These results revealed that AFB1 significantly induced hepatic mitochondrial antioxidant dysfunction. However, sodium selenite could significantly ameliorate
the negative effect induced by AFB1. 相似文献
20.
Jean Velours Alain Dautant Bndicte Salin Isabelle Sagot Daniel Brthes 《The international journal of biochemistry & cell biology》2009,41(10):1783-1789
The mitochondrial F1F0-ATP synthase adopts supramolecular structures. The interaction domains between monomers involve components belonging to the F0 domains. In Saccharomyces cerevisiae, alteration of these components destabilizes the oligomeric structures, leading concomitantly to the appearance of monomeric species of ATP synthase and anomalous mitochondrial morphologies in the form of onion-like structures. The mitochondrial ultrastructure at the cristae level is thus modified. Electron microscopy on cross-sections of wild type mitochondria display many short cristae with narrowed intra-cristae space, whereas yeast mutants defected in supramolecular ATP synthases assembly present a low number of large lamellar cristae of constant thickness and traversing the whole organelle. The growth of these internal structures leads finally to mitochondria with sphere-like structures with a mean diameter of 1 μm that are easily identified by epifluorescence microscopy. As a result, ATP synthase is an actor of the mitochondrial ultrastructure in yeast. This paper reviews the ATP synthase components whose modifications lead to anomalous mitochondrial morphology and also provides a schema showing the formation of the so-called onion-like structures. 相似文献