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1.
Conte da Frota ML Gomes da Silva E Behr GA Roberto de Oliveira M Dal-Pizzol F Klamt F Moreira JC 《Molecular and cellular biochemistry》2006,285(1-2):173-179
In this work we investigated the effects of retinoic acid (RA) in Sertoli cells. Sertoli cells isolated from 15-day-old Wistar rats were previously cultured for 48 h and then treated with RA for 24 h. RA at high doses (1–10 μM) increased TBARS levels and induced a decrease in cell viability. At low doses (0.1–100 nM) RA did not increase TBARS level. RA also did not increase cell death at these doses. In order to investigate changes in antioxidant defenses we measured the CAT, SOD and GPx activities in Sertoli cells treated with RA. Compared to control, RA increased around 200% SOD activity in all doses tested (0.1–100 nM); GPx activity was increased 407.49, 208.98 and 243.88% (0.1, 1 and 10 nM, respectively); CAT activity was increased 127% with RA 1 nM. To clarify if RA induces ROS production per se, we performed experiments in vitro using 2-deoxyribose as specific substrate of oxidative degradation by •OH radical as well as TRAP assay. RA at 10 μM increased 2-deoxyribose degradation, suggesting that some of the RA-induced effects are mediated via •OH formation. Furthermore, the total reactive antioxidant potential (TRAP) of the RA was determined. At low concentrations RA has induced no redox activity. Conversely, higher concentration of RA (1–10 μM) increased chemiluminescence. The chemiluminescence produced was directly proportional to radical generation. We provide, for the first time, evidence for a free radical generation by RA. Our results demonstrated that RA plays an important role in Sertoli cells and these effects appear to be mediated by ROS. 相似文献
2.
Cell suspension cultures of potato (Solanum tuberosum, cv. Tamasha) were treated with fusaric acid (FA), a nonspecific fungal toxin produced by Fusarium species to study the effects of FA on H2O2 generation, lipid peroxidation, and activities of antioxidant enzymes, i.e., superoxide dismutase (SOD), catalase, and ascorbate
peroxidase (APX). The toxicity of various FA doses was evaluated from viability of cultured cells of S. tuberosum. The toxic concentration of FA (10−3 M) reduced cell viability by 32% after 48-h incubation and induced alkalinization of the medium; the nontoxic concentration
of FA (10−6 M) had no effect on cell viability and pH of the culturing medium. The treatment of cells with FA caused rapid reversible
accumulation of H2O2 in cells, promoted lipid peroxidation, and elevated the activity of antioxidant enzymes. The toxic FA concentration elevated
the intracellular H2O2 content by 51–59% and stimulated lipid peroxidation rate by 35–40%. The nontoxic FA concentration raised the H2O2 content by 84–91% and enhanced lipid peroxidation rate by 18–24%. The addition of FA induced transient biphasic induction
of the antioxidant enzymes; the action of toxic and nontoxic concentrations differed in terms of the response amplitudes and
dynamics. The results confirm the well-known toxic impact of high doses of FA on the cultured cells, which is determined by
membrane transport disorders. In addition, the results reveal that toxic and nontoxic concentrations of FA are able to induce
pro- and antioxidant systems in the cultured cells of S. tuberosum. 相似文献
3.
Zekiye Sultan Altun Dilek Güneş Safiye Aktaş Zübeyde Erbayrktar Nur Olgun 《Neurochemical research》2010,35(3):437-443
The most widely used platinum-derived drug is cisplatin in neuroblastoma (NB) chemotherapy, which is severely neurotoxic.
Acetyl-l-Carnitine (ALC) is a natural occurring compound with a neuroprotective activity in several experimental paradigms. The aim
of this study was to determine the effects of ALC on cisplatin induced cytotoxicity and oxidative stress in NB cells. SH-SY5Y
(N-Myc negative) and KELLY (N-Myc positive) human NB cell lines were used. Cisplatin induced apoptosis was assessed by using
a Cell Death Detection ELISAPLUS kit. Lipid peroxidation levels were determined by HPLC analysis. Glutathione levels were determined spectrophotometrically.
ALC was used prophylactic or after cisplatin application. The level of cisplatin doses were determined in both type of NB
cells at which 50% cell death occurred along with synchronized apoptosis induced. Prophylactic 10 and 50 μmol of ALC concentrations
were decreased cisplatin induced lipid peroxidation compared to controls that normally exhibited apoptosis especially in SH-SY5Y
cells. Cisplatin caused oxidative stress through decreasing glutathione levels in both cell types. ALC were effectively inhibited
the increase in cisplatin induced oxidized glutathione and lipid peroxidation formation in NB cells. We suggested that prophylactic
ALC would be a useful agent for cisplatin induced toxicity in NB cells. 相似文献
4.
Jurate Savickiene Grazina Treigyte Ceslava Aleksandraviciene Ruta Navakauskiene 《Central European Journal of Biology》2010,5(5):600-612
The biological effects of low-dose radiation have attracted attention, but data are currently insufficient to fully understand
the beneficial role of the phenomenon. In the present study, we have investigated the effects of low doses of gamma-irradiation
alone and in combination with all-trans-retinoic acid (RA) on proliferation, apoptosis and differentiation of the human promyelocytic leukemia HL-60 cells. Changes
in cell behavior and protein expression were determined with the use of light and fluorescent microscopy, immunocytochemical
and Western blot analysis. Low-dose irradiation with 1–100 cGy caused a dose-dependent inhibition of HL-60 cell proliferation,
and induced apoptosis and differentiation to granulocytes with an increase in the number of CD15-positive cells. Pre-irradiation
with 1–100 cGy for 24 h before treatment with RA promoted apoptosis but did not impair RA-induced differentiation. Both processes
were associated with a decrease in the expression of the proliferating cell nuclear antigen (PCNA), BCL-2, c-MYC, and changes
in both cytosolic and nuclear levels of protein tyrosine-phosphorylation as well as protein kinase C alpha or beta isoforms.
These results demonstrate the beneficial role of low-dose irradiation in modulating leukemia cell proliferation, differentiation
and apoptosis. 相似文献
5.
Nadia Mushtaq Roberta Schmatz Luciane B. Pereira Mushtaq Ahmad Naiara Stefanello Juliano M. Vieira Fátima Abdalla Marília V. Rodrigues Jucimara Baldissarelli Luana Paula Pelinson Diéssica P. Dalenogare Karine Paula Reichert Eduardo M. Dutra Nádia Mulinacci Marzia Innocenti Maria Bellumori Vera Maria Morsch Maria Rosa Schetinger 《Cell biochemistry and function》2014,32(3):287-293
We investigated the efficacy of rosmarinic acid (RA) in preventing lipid peroxidation and increased activity of acetylcholinesterase (AChE) in the brain of streptozotocin‐induced diabetic rats. The animals were divided into six groups (n = 8): control, ethanol, RA 10 mg/kg, diabetic, diabetic/ethanol and diabetic/RA 10 mg/kg. After 21 days of treatment with RA, the cerebral structures (striatum, cortex and hippocampus) were removed for experimental assays. The results demonstrated that the treatment with RA (10 mg/kg) significantly reduced the level of lipid peroxidation in hippocampus (28%), cortex (38%) and striatum (47%) of diabetic rats when compared with the control. In addition, it was found that hyperglycaemia caused significant increased in the activity of AChE in hippocampus (58%), cortex (46%) and striatum (30%) in comparison with the control. On the other hand, the treatment with RA reversed this effect to the level of control after 3 weeks. In conclusion, the present findings showed that treatment with RA prevents the lipid peroxidation and consequently the increase in AChE activity in diabetic rats, demonstrating that this compound can modulate cholinergic neurotransmission and prevent damage oxidative in brain in the diabetic state. Thus, we can suggest that RA could be a promising compound in the complementary therapy in diabetes. Copyright © 2013 John Wiley & Sons, Ltd. 相似文献
6.
Sigolo CA Di Mascio P Kowaltowski AJ Garcia CC Medeiros MH 《Journal of bioenergetics and biomembranes》2008,40(2):103-109
Lipid peroxidation produces a large number of reactive aldehydes as secondary products. We have previously shown that the
reaction of cytochrome c with trans,trans-2,4-decadienal (DDE), an aldehyde generated as a product of lipid peroxidation in cell membranes, results in the formation
of adducts. Mass spectrometry analysis indicated that His-33, Lys-39, Lys-72 and Lys-100 in cytochrome c were modified by
DDE. In the present work, we investigated the effect of DDE on isolated rat liver mitochondria. DDE (162 μM) treatment increases
the rate of mitochondrial oxygen consumption. Extensive mitochondrial swelling upon treatment with DDE (900 nM–162 μM) was
observed by light scattering and transmission electron microscopy experiments. DDE-induced loss of inner mitochondrial membrane
potentials, monitored by safranin O fluorescence, was also observed. Furthermore, DDE-treated mitochondria showed an increase
in lipid peroxidation, as monitored by MDA formation. These results suggest that reactive aldehydes promote mitochondrial
dysfunction. 相似文献
7.
Effect of chromium on photosystem 2 in the unicellular green alga, <Emphasis Type="Italic">Chlorella pyrenoidosa</Emphasis> 总被引:2,自引:1,他引:1
We investigated the effect of chromium (20–40 g m−3, 8–72 h) on the photosystem 2 (PS2) activities of Chlorella pyrenoidosa cells. By using chlorophyll fluorescence transients, thermoluminescence, oxygen polarography, and Western blot analysis for
D1 protein we found that inhibition of PS2 can be accounted for by the enhanced photodestruction of the reaction centres in
the cells cultivated in the presence of Cr(VI) at 25 °C in “white light” (18 W m−2). Hence photodestruction of D1 is caused by an enhanced oxidative stress and lipid peroxidation, as indicated by the appearance
of a high-temperature thermoluminescence band. 相似文献
8.
Both α-lipoic acid (LA) and ascorbic acid (vitamin C) have been shown to improve endothelial dysfunction, a precursor of atherosclerosis.
Since oxidant stress can cause endothelial dysfunction, we tested the interaction and efficacy of these antioxidants in preventing
oxidant damage to lipids due to both intra- and extracellular oxidant stresses in EA.hy926 endothelial cells. LA spared intracellular
ascorbate in culture and in response to an intracellular oxidant stress induced by the redox cycling agent menadione. Extracellular
oxidant stress generated by incubating cells for 2 h in with 0.2 mg/ml LDL and 5 μM Cu2+ caused a time-dependent increase of the lipid peroxidation product malondialdehyde in both cells and LDL, preceded by rapid
disappearance of` α-tocopherol in LDL. α-Lipoic acid at concentrations of 40–80 μM blunted these effects. Similarly, intracellular
ascorbate concentrations of 1–2 mM also prevented Cu2+-induced lipid peroxidation in LDL and cells. Cu2+-dependent oxidation of LDL in the presence of ascorbate-loaded cells decreased intracellular ascorbate by 20%, but this decrease
was not reversed by LA. Both LA and ascorbate protect endothelial cells and LDL from either intra- or extracellular oxidant
stress, but that LA does not spare ascorbate in oxidatively stressed cells. 相似文献
9.
Proliferation and cellular aggregation are both crucial features for survival and self-renewal of primordial germ cells (PGCs).
Adhesive proteins play pivotal roles in cell–cell adhesion and signal exchanges under the influence of cytokines, growth factors
and bioactive metabolites such as retinoic acid (RA). In this study, proliferation-promoting effect of RA on chicken PGCs
was investigated by revealing changes in adhesive proteins E-cadherin and α/β catenins. PGCs were isolated from the genital
ridge of 4-day-old chicken embryos and cultured on embryonic fibroblast feeder. RA (10−7–10−5 M) increased PGCs aggregation and mRNA expression of E-cadherin and α/β-catenins. Furthermore, E-cadherin and β-catenin protein
expression levels were increased by RA treatment. However, RA-elicited effect was significantly attenuated by a PKC inhibitor
H7. In addition, the number and area of PGC colonies were increased by RA treatment at 10−7–10−5 M. Again, this increase was reduced by combined treatment of H7. The proliferating effect of RA on PGCs was further confirmed by increased mRNA expression of cyclins, CCND1 and CCNE1, and cyclin-dependent kinases 6 and 2, which are critical for G1–S progression in cell cycle. Moreover, flow cytometry analysis
confirmed that RA-treated PGC populations displayed a significant increase in the proportion of S and G2 phase cells. Likewise,
this stimulating action was hindered by combined H7 treatment. These results indicate that RA, as a bioactive metabolite of vitamin A, may promote PGC proliferation and increase
intercellular aggregation of PGCs via E-cadherin and α/β-catenins expression through the PKC signaling pathway. 相似文献
10.
The present study was undertaken to test the influence of exogenously applied traumatic acid (TA) upon the activity of several
antioxidant enzymes as well as lipid and protein peroxidation in green algae Chlorella vulgaris. Treatment with TA in concentration range of 10−6–10−5 M resulted in an increase of antioxidant enzyme (sodium dismutase, catalase, ascorbate peroxidase, NADH peroxidase, glutathione
reductase) activity. Moreover, TA suppressed lipid peroxidation and oxidative destruction of proteins belonging to the SH
groups. This data suggest that TA plays an important role in the metabolism of C. vulgaris and probably in its high ability to adapt to various environmental stress factors. 相似文献
11.
When wheat seedlings were grown in the presence of 62.5-500μM 4 chloro-5-dimethylamino-2-phenyl-3(2H) pyridazinone, an inhibitor of photosystem II electron transport, there was a marked
inhibition of in vivo photosystem II electron transport as revealed by the analysis of fast chlorophyll a fluorescence transients
in intact leaves and by the inhibition (95% at 500μM) of net photosynthesis in intact leaves Accompanying this inhibition of photosystem II electron transport, there was a decrease
in the content of photosynthetic pigments. The extent of lipid peroxidation, measured in terms of malondialdehyde content
was not increased; rather it was found decreased. An analysis of in vitro lipid peroxidation of the thylakoid membranes of
control and 4-chloro-5-dimethylamino-2-phenyl-3(2H) pyridazinone treated plants in the presence of a sensitizer dye (toluidine
blue) showed a similar rate both in the control and treated samples suggesting that the availability of unsaturated fatty
acids as a substrate for lipid peroxidation was not limiting even though it decreased in the treated plants. On the other
hand, it appears that the availability of the free radicals for lipid peroxidation was decreased byenhanced activity of the
enzyme systems involved in the metabolism of free radicals. Measurements of the activities of enzymes involved in the metabolism
of free radicals showed an increase in the activities of NADPH-glutathione reductase (6–8 fold) and catalase (15–30%) and
a decrease in the activity of superoxide dismutase (30–45%) in the treated plants. 相似文献
12.
We have investigated the neuroprotective effect of sesaminol glucosides (SG) in SK-N-SH cells. SG prevented apoptotic cell
death induced by Aβ25–35. In parallel, SK-N-SH cells exposed to Aβ25–35 underwent oxidative stress as shown by the elevated level of intracellular ROS, lipid peroxidation, and 8-hydroxy-2′-deoxyguanosine
(8-OHdG) formation, which were effectively suppressed by SG treatment. Furthermore, SG reversed the activities of catalase
and glutathione peroxidase, and restored intracellular GSH levels in Aβ25–35 challenged SK-N-SH cells. In addition, SG inhibited not only Aβ25–35-induced apoptotic features including cleavage of poly(ADP-ribose) polymerase, activation of caspase-3, and activation of
caspase-9, but also elevated Bax/Bcl-2 ratio in SK-N-SH cells treated with Aβ25–35. It was also observed that Aβ25–35 stimulated the phosphorylation of mitogen-activated protein kinases (MAPKs), including extracellular protein regulated protein
kinase (ERK), c-Jun N-terminal kinase (JNK), and p38 MAP kinase. SG inhibited phosphorylation of the JNK, ERK and p38 MAP
kinase. These results suggest that SG has a protective effect against Aβ25–35-induced neuronal apoptosis, possibly through scavenging oxidative stress and regulating MAPKs signaling pathways. 相似文献
13.
Abib RT Quincozes-Santos A Nardin P Wofchuk ST Perry ML Gonçalves CA Gottfried C 《Molecular and cellular biochemistry》2008,310(1-2):153-158
There is a current interest in dietary compounds, such as green tea polyphenols, that can favor protection against a variety
of brain disorders, including Alzheimer’s disease, ischemia, and stroke. The objective of the present study was to investigate
the effects of (_)-epicatechin-3-gallate (ECG), one of three three major green tea antioxidants, on C6 lineage cells. Here, we evaluated cell
morphology and integrity and specific astrocyte activities; glutamate uptake and secretion of S100B in the presence of 0.1,
1 and 10 μM ECG. During 6 h of incubation, cell morphology was altered only at 10 μM ECG; however, after 24 h of treatment,
cells become stellate in the presence of all concentrations of ECG. Loss of cell integrity was observed after 24 h with 10 μM
ECG and represented only 6% of cells, in contrast with 2% observed at basal conditions. ECG (1–10 μM) induced a decrease (about
36%) in glutamate uptake after 1 h of incubation. After 6 h, an opposite effect occurred and ECG induced a sustained increase
in glutamate uptake of about 70% from 0.1 μM. In addition, a significant increase in S100B was observed at 1 μM ECG (36%)
and 10 μM ECG (69%) after 1 h, in contrast to 6 h of treatment, where all doses of ECG induced a significant increase (about
60%) in S100B secretion. These data demonstrate that ECG induces a significant improvement in glutamate uptake and S100B secretion
in C6 cells, indicating that ECG could contribute to the neuroprotective role of astroglial cells. 相似文献
14.
Eicosapentaenoic acid (EPA) is one of the major dietary polyunsaturated fatty acids and induces apoptosis in several cancer
cells. In this study, the EPA induced lipid peroxidation and response of antioxidative enzymes have been investigated in rat
pheochromocytoma PC12 cells to elucidate the mechanisms of apoptosis induced by the polyunsaturated fatty acid EPA. We have
analyzed superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPX) activities and glutathione (GSH) contents
in PC12 cells after exposure to different concentrations of EPA. Lipid peroxidation was shown to increase in the presence
of EPA as an indication of the oxidative damage. Lipid peroxidation was enhanced by EPA in a dose-dependent manner, and the
loss of cell viability was partially reversed by vitamin E. In the case of antioxidant enzyme activities, SOD and GPX activities
and GSH contents increased significantly at 50 μmol/L EPA and were respectively 2.41-fold (p < 0.01), 3.49-fold (p < 0.05), and 1.43-fold (p < 0.05) higher than controls. The CAT activity at 10 μmol/L had the highest value and was increased by 25.83% (p < 0.05) compared to control. The results suggest that in PC12 cells the mechanism of apoptosis induced by EPA may be partly
due to lipid peroxidation. 相似文献
15.
16.
Farshad Malihi Azadeh Hosseini-Tabatabaei Hadi Esmaily Reza Khorasani Maryam Baeeri Mohammad Abdollahi 《Central European Journal of Biology》2009,4(3):369-380
Type 1 diabetes mellitus (T1DM) is characterized by an impairment of the insulin-secreting beta cells with an immunologic
base. Inflammatory cytokines such as tumor necrosis factor (TNF)-α and interleukin (IL)-1β, and free radicals are believed
to play key roles in destruction of pancreatic β cells. The present study was designed to investigate the effect of Silybum marianum seed extract (silymarin), a combination of several flavonolignans with immunomodulatory, anti-oxidant, and anti-inflammatory
potential on streptozotocin (STZ)-induced T1DM in mouse. Experimental T1DM was induced in male albino mice by IV injection
of multiplelow- doses of STZ for 5 days. Seventy-two male mice in separate groups received various doses of silymarin (20,
40, and 80 mg/kg) concomitant or after induction of diabetes for 21 days. Blood glucose and pancreatic biomarkers of inflammation
and toxic stress (IL-1β, TNF-α, myeloperoxidase, lipid peroxidation, protein oxidation, thiol molecules, and total antioxidant
capacity) were determined. Silymarin treatment reduced levels of inflammatory cytokines such as TNF-α and IL-1β and oxidative
stress mediators like myeloperoxidase activity, lipid peroxidation, carbonyl and thiol content of pancreatic tissue in an
almost dose dependent manner. No marked difference between the prevention of T1DM and the reversion of this disease by silymarin
was found. Use of silymarin seems to be helpful in T1DM when used as pretreatment or treatment. Benefit of silymarin in human
T1DM remains to be elucidated by clinical trials. 相似文献
17.
Chinese hamster V79 cells were conditioned by repeated treatment with low doses of hydrogen peroxide. After this treatment,
the conditioned cells were compared to parental V79 cells with regard to different endpoints. It was found that, compared
to parental cells, the conditioned cells tolerated low serum concentrations better, they suffered from higher levels of aneuploidy,
and they showed enhanced antioxidant defense. When exposed to γ-rays, they suffered from lipid peroxidation to a lesser extent,
were more resistant to cell killing, exhibited higher mutation frequency at the HGPRT locus, and showed lower frequency of
apoptosis. These cells also induced antioxidant enzymes in response to γ-ray exposure that differently was from than the parental
cells. Overall, the data suggest a stable adaptive response in the conditioned cells. 相似文献
18.
Yong Soo Lee Da-Qing Jin Seung Hee Park Soon Young Han Hyung Sik Kim Tae Cheon Jeong 《Free radical research》2013,47(12):1283-1289
Oxidative stress has been known to be involved in the mechanism of toxic effects of various agents on many cellular systems. In this study we investigated the role of reactive oxygen species (ROS) in 2,3,7,8-tetrachlorodibenzo- p -dioxin (TCDD)-induced neuronal cell toxicity using SK-N-SH human neuroblastoma cells. TCDD inhibited proliferation of the cells in a dose-dependent manner, which was revealed by MTT staining, counting of cells stained with trypan blue and [ 3 H]thymidine uptake assay. TCDD also suppressed the basal generation of ROS in a time- and concentration-dependent manner assessed by 2',7'-dichlorofluorescein fluorescence. In addition, TCDD induced a dose-dependent inhibition of lipid peroxidation, a biomarker of oxidative stress, whereas it significantly increased the level of glutathione (GSH), an intracellular free radical scavenger in the cells. Moreover, TCDD altered the activities of major antioxidant enzymes; increase in superoxide dismutase (SOD) and catalase, but decrease in glutathione peroxidase (GSH-Px) and glutathione reductase (GSH-Red). Pretreatment with l -buthionine- S , R -sulfoximine (BSO, 50 w M), an inhibitor of GSH synthesis, significantly prevented the TCDD-induced reduction in lipid peroxidation and cell proliferation. Interestingly, exogenous application of an oxidant, H 2 O 2 (50 w M) markedly restored the inhibited cell proliferation induced by TCDD. Taken together, these results suggest that alteration of cellular redox balance may mediate the TCDD-induced inhibition of proliferation in human neuronal cells. 相似文献
19.
Recently we have demonstrated that extracellular ATP acts as an excitatory neurotransmitter and enhances cell death in the
presence of ferrous ions. By using a newly developed cis-parinaric acid fluorescence technique, we demonstrated that ATP,
in a dose dependent manner, enhanced the increased membrane lipid peroxidation in PC12 cells when cells were incubated with
micromolar FeCl2/DTP. P2 purinoceptor agonists, α,β-methylene ATP and 2-methylthio-ATP, induced PC12 cell lipid peroxidation, but to a lesser extent
than ATP. ATP-induced Ca2+ influx via P2 purinoceptor activation significantly increased the intracellular Ca2+ concentration, which may have triggered a free radical generating cascade(s), and led to membrane lipid peroxidation and
cell death. Since oxidative stress has been implicated in certain neurodegenerative diseases such as aging, extracellular
ATP may contribute to neuronal cell death by an oxidative mechanism involving lipid peroxidation. 相似文献
20.
This study aimed to evaluate the antioxidant activities of a cultured medicinal fungus—Armillariella mellea (Vahl. ex Fr.) Karst. (AM). Three antioxidant assay systems, namely cytochrome c, xanthine oxidase inhibition, and FeCl2-ascorbic acid stimulated lipid peroxidation in rat tissue homogenate tests, were used. Total flavonoid and phenol contents
of AM extracts were also analyzed. Results showed that both aqueous (AM-H2O) and ethanolic (AM-EtOH) extracts of solid state cultured AM showed antioxidant activities in a concentration-dependent
manner. At concentrations 1–100 μg/ml, the free radical scavenging activity was 73.7–92.1% for AM-H2O, and 60.0–90.8% for AM-EtOH. These extracts also showed an inhibitory effect on xanthine oxidase activity, but with a lesser
potency (IC50 is 9.17 μg/ml for AM-H2O and 7.48 μg/ml for AM-EtOH). In general, AM-H2O showed a stronger antilipid peroxidation activity on different rat’s tissues than AM-EtOH. However, both AM extracts displayed
a weak inhibitory effect on lipid peroxidation in plasma. Interestingly, the antilipid peroxidation activity of AM-H2O (IC50–6.66 μg/ml) in brain homogenate was as good as IC50–5.42 μg/ml. AM-H2O (80.0 mg/g) possessed a significantly higher concentration of total flavonoids than AM-EtOH (30.0 mg/g), whereas no difference
was noted in the total phenol content between these two extracts. These results conclude that AM extracts possess potent free
radical scavenging and antilipid peroxidation activities, especially the AM-H2O in the brain homogenate.
Published in Russian in Prikladnaya Biokhimiya i Mikrobiologiya, 2007, Vol. 43, No. 4, pp. 495–500.
The text was submitted by the authors in English. 相似文献