共查询到20条相似文献,搜索用时 31 毫秒
1.
Kwang Sik Suh Suk Chon Seungjoon Oh Sung Woon Kim Jin-Woo Kim Young Seol Kim Jeong-Taek Woo 《Cell biology and toxicology》2010,26(3):189-199
Epigallocatechin-3-gallate (EGCG) is the main polyphenolic constituent in green tea and is believed to function as an antioxidant.
However, increasing evidence indicates that EGCG produces reactive oxygen species (ROS) and subsequent cell death. In this
study, we investigated the prooxidative effects of EGCG on the HIT-T15 pancreatic beta cell line. Dose-dependent cell viability
was monitored with the cell counting kit-8 assay, while the induction of apoptosis was analyzed by a cell death ELISA kit
and comet assay. Extracellular H2O2 was determined using the Amplex Red Hydrogen Peroxide Assay Kit. Intracellular oxidative stress was measured by fluorometric
analysis of 2′,7′-dichlorofluorescin (DCFH) oxidation using DCFH diacetate (DA) as the probe. Treatment with EGCG (5–100 μM)
decreased the viability of pancreatic beta cells, caused concomitant increases in apoptotic cell death, and increased the
production of H2O2 and ROS. Catalase, the iron-chelating agent diethylenetriaminepentaacetic acid, and the Fe(II)-specific chelator o-phenanthroline all suppressed the effects of EGCG, indicating the involvement of both H2O2 and Fe(II) in the mechanism of action of EGCG. The antioxidant N-acetyl-cysteine and alpha-lipoic acid also suppressed the effects of EGCG. Furthermore, EGCG did not scavenge exogenous H2O2, but rather, it synergistically increased H2O2-induced oxidative cell damage in pancreatic beta cells. Together, these findings suggest that in the HIT-T15 pancreatic beta
cell line, EGCG mediated the generation of H2O2, triggering Fe(II)-dependent formation of a highly toxic radical that in turn induced oxidative cell damage. 相似文献
2.
Maarten Van der Heggen Sara Martins Gisela Flores Eduardo V. Soares 《Applied microbiology and biotechnology》2010,88(6):1355-1361
The effect of Pb on Saccharomyces cerevisiae cell structure and function was examined. Membrane integrity was assessed by the release of UV-absorbing compounds and by
the intracellular K+ efflux. No leakage of UV260-absorbing compounds or loss of K+ were observed in Pb (until 1,000 μmol/l) treated cells up to 30 min; these results suggest that plasma membrane seems not
to be the immediate and primary target of Pb toxicity. The effect of Pb on yeast metabolism was examined using the fluorescent
probe FUN-1 and compared with the ability to reproduce, evaluated by colony-forming units counting. The exposition of yeast
cells, during 60 min to 1,000 μmol/l Pb, induces a decrease in the ability to process FUN-1 although the cells retain its
proliferation capacity. A more prolonged contact time (120 min) of yeast cells with Pb induces a marked (> 50%) loss of yeast
cells metabolic activity and replication competence through a mechanism which most likely requires protein synthesis. 相似文献
3.
Western lifestyle plays an important role in the prevalence of type 2 diabetes by causing insulin resistance and pancreatic
β-cell dysfunction, a prerequisite for the development of diabetes. High fat diet and alcohol are major components of the
western diet. The aim of the present study was to investigate the effects of ethanol and fatty acids on β-cell survival and
metabolism. We treated the rat β-cell line RINm5F with ethanol, a mixture of palmitic and oleic acids, or both. Reactive oxygen
species (ROS) were determined by (5-(and-6)-chloromethyl-2′,7′-dichlorodihydrofluorescein diacetate) (CM-H2DCFDA) fluorescence
assay, and mitochondrial activity was assessed by 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyl tetrazolium bromide (MTT) reduction
assay and by determining ATP production. Cell viability was assessed with a cell counter and trypan blue exclusion, and the
mode of cell death by Hoechst33342 and propidium iodide staining. With both ethanol and fatty acid treatments, MTT reduction
and ATP production decreased, whereas ROS production increased. Ethanol treatment had no effect on cell number, whereas fatty
acid treatment reduced the cell number. Cell incubation with ethanol, fatty acids, or both increased the number of Hoechst
33342-positive nuclei. However, the majority of nuclei from fatty acid-treated cells were stained with propidium iodide, indicating
a loss of plasma membrane integrity. We conclude that both ethanol and fatty acids generate cellular oxidative stress, and
affect mitochondrial function in RINm5F β-cells. However, ethanol causes β-cell death by apoptosis, whereas fatty acids cause
cell death predominantly by necrosis. It is not known whether these results are applicable to human β-cells. 相似文献
4.
The molecular mechanisms involved in the ability of yeast cells to adapt and respond to oxidative stress are of great interest
to the pharmaceutical, medical, food, and fermentation industries. In this study, we investigated the time-dependent, cellular
redox homeostasis ability to adapt to menadione-induced oxidative stress, using biochemical and proteomic approaches in Saccharomyces cerevisiae KNU5377. Time-dependent cell viability was inversely proportional to endogenous amounts of ROS measured by a fluorescence
assay with 2′,7′-dichlorofluorescin diacetate (DCFHDA), and was hypersensitive when cells were exposed to the compound for
60 min. Morphological changes, protein oxidation and lipid peroxidation were also observed. To overcome the unfavorable conditions
due to the presence of menadione, yeast cells activated a variety of cell rescue proteins including antioxidant enzymes, molecular
chaperones, energy-generating metabolic enzymes, and antioxidant molecules such as trehalose. Thus, these results show that
menadione causes ROS generation and high accumulation of cellular ROS levels, which affects cell viability and cell morphology
and there is a correlation between resistance to menadione and the high induction of cell rescue proteins after cells enter
into this physiological state, which provides a clue about the complex and dynamic stress response in yeast cells. 相似文献
5.
Inhibitor studies and mutant analysis revealed a C30 pathway via 4,4′-diapophytoene and 4,4′-diaponeurosporene to 4,4′-diaponeursoporene-4-oic acid esters related to staphyloxanthin
in Halobacillus halophilus. Six genes may be involved in this biosynthetic pathway and could be found in two adjacent gene clusters. Two genes of this
pathway could be functionally assigned by functional pathway complementation as a 4,4′-diapophytoene synthase and a 4,4′-diapophytoene
desaturase gene. These genes were organized in two operons together with two putative oxidase genes, a glycosylase and an
acyl transferase ortholog. Pigment mutants were obtained by chemical mutagenesis. Carotenoid analysis showed that a white
mutant accumulated 4,4′-diapophytoene due to a block in desaturation. In a yellow mutant carotenogenesis was blocked at the
stage of 4,4′-diaponeurosporene and in an orange mutant at the stage of 4,4′-diaponeurosporene-4-oic acid. The protective
function of these pigments could be demonstrated for H. halophilus after inhibition of carotenoid synthesis by initiation of oxidative stress. A degree of oxidative stress which still allowed
50% growth of carotenogenic cells resulted in the death of the cells devoid of colored carotenoids. 相似文献
6.
Nzengue Y Steiman R Rachidi W Favier A Guiraud P 《Biological trace element research》2012,146(3):410-419
In this report, we have investigated the role of copper (Cu) and zinc (Zn) in oxidative stress induced by cadmium (Cd) in
C6 cells. Cells were exposed to 20 μM Cd, 500 μM Cu, and 450 μM Zn for 24 h. Then, toxic effects, cellular metals levels,
oxidative stress parameters, cell death, as well as DNA damage were evaluated. Cd induced an increase in cellular Cd, Cu,
and Zn levels. This results not only in the inhibition of GSH-Px, GRase, CAT, and SOD activities but also in ROS overproduction,
oxidative damage, and apoptotic cell death not related to Cu and Zn mechanisms. The thiol groups and GSH levels decreased,
whereas the lipid peroxidation and DNA damage increased. The toxicity of Zn results from the imbalance between the inhibition
of antioxidant activities and the induction of MT synthesis. The increase in Cu and Zn levels could be explained by the disruption
of specific transporter activities, Cd interference with signaling pathways, and metal displacement. Our results suggest that
the alteration of Cu and Zn homeostasis is involved in the oxidative stress induced by Cd. 相似文献
7.
Bhushan S Kumar A Malik F Andotra SS Sethi VK Kaur IP Taneja SC Qazi GN Singh J 《Apoptosis : an international journal on programmed cell death》2007,12(10):1911-1926
A triterpenediol (TPD) comprising of isomeric mixture of 3α, 24-dihydroxyurs-12-ene and 3α, 24-dihydroxyolean-12-ene from
Boswellia serrata induces apoptosis in cancer cells. An attempt was made in this study to investigate the mechanism of cell death by TPD in
human leukemia HL-60 cells. It inhibited cell proliferation with IC50 ∼ 12 μg/ml and produced apoptosis as measured by various biological end points e.g. increased sub-G0 DNA fraction, DNA ladder
formation, enhanced AnnexinV-FITC binding of the cells. Further, initial events involved massive reactive oxygen species (ROS)
and nitric oxide (NO) formation, which were significantly inhibited by their respective inhibitors. Persistent high levels
of NO and ROS caused Bcl-2 cleavage and translocation of Bax to mitochondria, which lead to loss of mitochondrial membrane
potential (Δψm) and release of cytochrome c, AIF, Smac/DIABLO to the cytosol. These events were associated with decreased expression of
survivin and ICAD with attendant activation of caspases leading to PARP cleavage. Furthermore, TPD up regulated the expression
of cell death receptors DR4 and TNF-R1 level, leading to caspase-8 activation. These studies thus demonstrate that TPD produces
oxidative stress in cancer cells that triggers self-demise by ROS and NO regulated activation of both the intrinsic and extrinsic
signaling cascades. 相似文献
8.
Calabrese V Cornelius C Maiolino L Luca M Chiaramonte R Toscano MA Serra A 《Neurochemical research》2010,35(12):2208-2217
Ménière’s disease (MD) is characterized by the triad of fluctuating hearing loss, episodic vertigo and tinnitus, and by endolymphatic
hydrops found on post-mortem examination. Increasing evidence suggests that oxidative stress is involved in the development
of endolymphatic hydrops and that cellular damage and apoptotic cell death might contribute to the sensorineural hearing loss
found in later stages of MD. While excess reactive oxygen species (ROS) are toxic, regulated ROS, however, play an important
role in cellular signaling. The ability of a cell to counteract stressful conditions, known as cellular stress response, requires
the activation of pro-survival pathways and the production of molecules with anti-oxidant, anti-apoptotic or pro-apoptotic
activities. Among the cellular pathways conferring protection against oxidative stress, a key role is played by vitagenes,
which include heat shock proteins (Hsps) as well as the thioredoxin/thioredoxin reductase system. In this study we tested
the hypothesis that in MD patients measurable increases in markers of cellular stress response and oxidative stress in peripheral
blood are present. This study also explores the hypothesis that changes in the redox status of glutathione, the major endogenous
antioxidant, associated with abnormal expression and activity of carbonic anhydrase can contribute to increase oxidative stress
and to disruption of systemic redox homeostasis which can be associated to possible alterations on vulnerable neurons such
as spiral ganglion neurons and consequent cellular degeneration. We therefore evaluated systemic oxidative stress and cellular
stress response in patients suffering from Meniere’s disease (MD) and in age-matched healthy subjects. Systemic oxidative
stress was estimated by measuring protein oxidation, such as protein carbonyls (PC) and 4-hydroxynonenal (HNE) in lymphocytes
of MD patients, as well as ultraweak luminescence (UCL) as end-stable products of lipid oxidation in MD plasma and lymphocytes,
as compared to age-matched controls, whereas heat shock proteins Hsp70 and thioredoxin (Trx) expression were measured in lymphocytes
to evaluate the systemic cellular stress response. Increased levels of PC (P < 0.01) and HNE (P < 0.05) have been found in lymphocytes from MD patients with respect to control group. This was paralleled by a significant
induction of Hsp70, and a decreased expression of Trx (P < 0.01), whereas a significant decrease in both plasma and lymphocyte ratio reduced glutathione GSH) vs. oxidized glutathione
(GSSG) (P < 0.05) were also observed. In conclusion, patients affected by MD are under condition of systemic oxidative stress and the
induction of vitagenes Hsp70 is a maintained response in counteracting the intracellular pro-oxidant status generated by decreased
content of GSH as well as expression of Trx. The search for novel and more potent inducers of vitagenes will facilitate the
development of pharmacological strategies to increase the intrinsic capacity of vulnerable ganglion cells to maximize antidegenerative
mechanisms, such as stress response and thus cytoprotection. 相似文献
9.
Sivalokanathan S Ilayaraja M Balasubramanian MP 《Molecular and cellular biochemistry》2006,286(1-2):87-93
Role of oxidative stress and Na+,K+-ATPase in the cytotoxicity of hexachlorocyclohexane (HCH) on Ehrlich Ascites tumor (EAT) cells has been studied. HCH caused dose dependent cell death as measured by trypan blue exclusion and lactate dehydrogenase (LDH) leakage from the cells. HCH induced oxidative stress in EAT cells which was characterized by glutathione depletion, lipid peroxidation (LPO), reactive oxygen species (ROS) production and inhibition of antioxidant enzymes, superoxide dismutase (SOD) and catalase (CAT). Protective effect of antioxidants on HCH induced oxidative stress was assessed, among the antioxidants used only quercetin inhibited HCH-induced LPO and ROS production as well as cell death whereas α -tocopherol, ascorbic acid and BHA inhibited LPO but not cell death. Inhibition of membrane bound Na+,K+-ATPase was a characteristic feature of HCH cytotoxicity in EAT cells. Experimental evidence indicates that HCH-induced cell death involves oxidative stress due to ROS production and membrane perturbation in EAT cells. 相似文献
10.
The effects of trans fatty acids, elaidic acid (trans-9, C18:1) and linoelaidic acid (trans-9, trans-12 C18:2), at 20 or 40 μM
in nerve growth factor differentiated PC12 cells with or without beta-amyloid peptide (Aβ) were examined. Elaidic acid treatment
alone did not affect cell viability and oxidative injury associated markers (P > 0.05). However, co-treatments of elaidic acid and Aβ led to more reduction in mitochondrial membrane potential (MMP) and
Na+-K+-ATPase activity, and more increase in DNA fragmentation and 8-hydroxydeoxyguanosine (8-OHdG) production than Aβ treatment
alone (P < 0.05). Linoelaidic acid alone exhibited apoptotic and oxidative effects in cells via decreasing MMP and Na+-K+-ATPase activity, increasing reactive oxygen species (ROS) level, lowering glutathione content and glutathione peroxidase
(GPX) activity (P < 0.05). The co-treatments of linoelaidic acid with Aβ further enhanced oxidative damage via enhancing the generation of
ROS, nitrite oxide and 8-OHdG, elevating caspase-3, caspase-8 and nitric oxide synthase activities, as well as declining GPX,
catalase and superoxide dismutase activities (P < 0.05). These results suggested that the interaction of linoelaidic acid and Aβ promoted oxidative stress and impaired mitochondrial
functions in neuronal cells. 相似文献
11.
M. O. Emel’yanov Yu. A. Kim A. F. Korystova L. N. Kublik V. V. Shaposhnikova Yu. N. Korystov 《Biochemistry (Moscow) Supplemental Series A: Membrane and Cell Biology》2010,4(2):212-219
The effect of a short-time (1 h) oxidative stress on multidrug resistance (MDR) of murine leukemic P388VR cells has been investigated.
We studied the production of reactive oxygen species (ROS) in cells depending on the composition of medium and the concentration
of cells and hydrogen peroxide, as well as the effect of hydrogen peroxide on MDR of cells. MDR was determined from the transport
of calcein acetoxymethyl ester out of the cells and from a change in cell sensitivity to vincristine. The amount of ROS arising
in cells was determined using 2′,7′-dichlorodihydrofluorescein diacetate (DCFH2-DA). It was shown that the rate of ROS formation in cells decreases after the addition of serum to the medium and with an
increase of the cell number. By the action of hydrogen peroxide, the amount of ROS increases directly with its concentration.
Oxidative stress generated by 30–300 μM hydrogen peroxide decreases the MDR of the cells. The effect of hydrogen peroxide
increases with the treatment duration and concentration of hydrogen peroxide. MDR determined by the criterion of the efflux
of calcein ester from cells is completely suppressed after 1-h exposure to 300 μM hydrogen peroxide. At a concentration of
hydrogen peroxide of 60 μM and treatment duration of 1 h, the sensitivity of P388VR cells to vincristine increases to reach
the sensitivity of the wild-type P388 cells. Rapid (about 1 h) suppression of MDR is caused by inhibition of the activity
of transport proteins. MDR decrease induced by oxidative stress can be used in therapy of tumors resistant to anticancer drugs. 相似文献
12.
Jung Jin Hwang Ha Na Kim Jean Kim Dong-Hyung Cho Mi Joung Kim Yong-Sook Kim Yunha Kim Sung-Jin Park Jae-Young Koh 《Biometals》2010,23(6):997-1013
Treatment of MCF-7 cells with tamoxifen induced vacuole formation and cell death. Levels of the autophagy marker, microtubule-associated
protein light chain 3 (LC3)-II also increased, and GFP-LC3 accumulated in and around vacuoles in MCF-7 cells exposed to tamoxifen,
indicating that autophagy is involved in tamoxifen-induced changes. Live-cell confocal microscopy with FluoZin-3 staining
and transmission electron microscopy with autometallographic staining revealed that labile zinc(II) ion (Zn2+) accumulated in most acidic LC3(+) autophagic vacuoles (AVs). Chelation of Zn2+ with N,N,N′,N′-tetrakis (2-pyridylmethyl) ethylenediamine (TPEN) blocked the increase in phospho-Erk and LC3-II levels, and attenuated
AV formation and cell death. Conversely, the addition of ZnCl2 markedly potentiated tamoxifen-induced extracellular signal-regulated kinase (Erk) activation, autophagy and cell death,
indicating that Zn2+ has an important role in these events. Tamoxifen-induced death was accompanied by increased oxidative stress and lysosomal
membrane permeabilization (LMP) represented as release of lysosomal cathepsins into cytosol. Treatment with the antioxidant
N-acetyl-l-cysteine (NAC) blunted the increase in Zn2+ levels and reduced LC3-II conversion, cathepsin D release and cell death induced by tamoxifen. And cathepsin inhibitors attenuated
cell death, indicating that LMP contributes to tamoxifen-induced cell death. Moreover, TPEN blocked tamoxifen-induced cathepsin
D release and increase in oxidative stress. The present results indicate that Zn2+ contributes to tamoxifen-induced autophagic cell death via increase in oxidative stress and induction of LMP. 相似文献
13.
Oxidised low density lipoprotein (oxLDL) is thought to be a significant contributor to the death of macrophage cells observed in advanced atherosclerotic plaques. Using human-derived U937 cells we have examined the effect of cytotoxic oxLDL on oxidative stress and cellular catabolism.Within 3 h of the addition of oxLDL, there was a rapid, concentration dependent rise in cellular reactive oxygen species followed by the loss of cellular GSH, and the enzyme activity of both glyceraldehyde 3-phosphate dehydrogenase (GAPDH) and aconitase. The loss of these catabolic enzymes was accompanied by the loss of cellular ATP and lower lactate generation. Addition of the macrophage antioxidant 7,8-dihydroneopterin inhibited the ROS generation, glutathione loss and catabolic inactivation. NOX was shown to be activated by oxLDL addition while apocynin inhibited the loss of GSH and cell viability. The data suggests that oxLDL triggers an excess of ROS production through NOX activation, and catabolic failure through thiol oxidation resulting in cell death. 相似文献
14.
Role of Oxidative Stress,Apoptosis, and Intracellular Homeostasis in Primary Cultures of Rat Proximal Tubular Cells Exposed to Cadmium 总被引:1,自引:0,他引:1
Cadmium (Cd) is a known nephrotoxic element. In this study, the primary cultures of rat proximal tubular (rPT) cells were
treated with low doses of cadmium acetate (2.5 and 5 μM) to investigate its cytotoxic mechanism. A progressive loss in cell
viability, together with a significant increase in the number of apoptotic and necrotic cells, were seen in the experiment.
Simultaneously, elevation of intracellular [Ca2+]i and reactive oxygen species (ROS) levels, significant depletion of mitochondrial membrane potential(Δ
Ψ) and cellular glutathione (GSH), intracellular acidification, and inhibition of Na+, K+-ATPase and Ca2+-ATPase activities were revealed in a dose-dependent manner during the exposure, while the cellular death and the apoptosis
could be markedly reversed by N-acetyl-l-cysteine (NAC). Also, the calcium overload and GSH depletion were significantly affected by NAC. In conclusion, exposure
of rPT cells to low-dose cadmium led to cellular death, mediated by an apoptotic and a necrotic mechanism. The apoptotic death
might be the chief mechanism, which may be mediated by oxidative stress. Also, a disorder of intracellular homeostasis induced
by oxidative stress and mitochondrial dysfunction is a trigger of apoptosis in rPT cells. 相似文献
15.
AIM To identify and characterize the protective effect that L-carnitine exerted against an oxidative stress in C2C12 cells.METHODS Myoblastic C2C12 cells were treated with menadione, a vitamin K analog that engenders oxidative stress, and the protective effect of L-carnitine(a nutrient involved in fatty acid metabolism and the control of the oxidative process), was assessed by monitoring various parameters related to the oxidative stress, autophagy and cell death. RESULTS Associated with its physiological function, a muscle cell metabolism is highly dependent on oxygen and may produce reactive oxygen species(ROS), especially under pathological conditions. High levels of ROS are known to induce injuries in cell structure as they interact at many levels in cell function. In C2C12 cells, a treatment with menadione induced a loss of transmembrane mitochondrial potential, an increase in mitochondrial production of ROS; it also induces autophagy and was able to provoke cell death. Pre-treatment of the cells with L-carnitine reduced ROS production, diminished autophagy and protected C2C12 cells against menadione-induced deleterious effects. CONCLUSION In conclusion, L-carnitine limits the oxidative stress in these cells and prevents cell death. 相似文献
16.
It has been documented that medical prosthetic alloys release metal ions into surrounding tissues and cause cytotoxicity,
but the mechanisms remain undefined. In that regard the cellular oxidative stress may be a common pathway in cellular responses
to metal ions. The objective of this study was to approach the hypothesis that oxidative stress mediates chromium-induced
cytotoxicity in rat calvarial osteoblasts. Osteoblasts were exposed to different concentrations of Cr6+ or Cr3+ (5–20 μM) in the presence or absence of the antioxidant N-acetyl-cysteine (NAC; 1–5 mM). Cellular viability, differentiation, and intracellular ultrastructural alterations were evaluated
by MTT assay, alkaline phosphatase (ALP) activity assay, and transmission electron microscopy. Cellular oxidative stress was
evaluated by intracellular reactive oxygen species (ROS) production. ROS production was monitored by the oxidation-sensitive
fluorescent probe 2′7′-dichlorofluorescin diacetate (DCFH-DA). A time- and concentration- dependent increased cytotoxicity,
time-dependent increased intracellular ROS production were indicated on exposure to Cr6+. Pretreatment of osteoblasts with 1–5 mM NAC afforded dose-dependent cytoprotective effects against Cr6+-induced cytotoxicity in osteoblasts. NAC decreased the level of intracellular ROS induced by Cr6+, too. While Cr3+ and NAC did not have any significant effects on osteoblasts (5–20 μM). These results suggest that oxidative stress is involved
in Cr6+-induced cytotoxicity in osteoblasts, and NAC can provide protection for osteoblasts against Cr6+-induced oxidative stress. Cr3+ (5–20 μM) have no significant cytotoxicity in osteoblasts based on the results of this study. 相似文献
17.
S. H. Mousavi Z. Tayarani-Najaran M. Asghari H. R. Sadeghnia 《Cellular and molecular neurobiology》2010,30(4):591-598
The serum/glucose deprivation (SGD)-induced cell death in cultured PC12 cells represents a useful in vitro model for the study
of brain ischemia and neurodegenerative disorders. Nigella sativa L. (family Ranunculaceae) and its active component thymoquinone (TQ) has been known as a source of antioxidants. In the present
study, the protective effects of N. sativa and TQ on cell viability and reactive oxygen species (ROS) production in cultured PC12 cells were investigated under SGD
conditions. PC12 cells were cultured in DMEM medium containing 10% (v/v) fetal bovine serum, 100 units/ml penicillin, and
100 μg/ml streptomycin. Cells were seeded overnight and then deprived of serum/glucose for 6 and 18 h. Cells were pretreated
with different concentrations of N. sativa extract (15.62–250 μg/ml) and TQ (1.17–150 μM) for 2 h. Cell viability was quantitated by MTT assay. Intracellular ROS production
was measured by flow cytometry using 2′,7′-dichlorofluorescin diacetate (DCF-DA) as a probe. SGD induced significant cells
toxicity after 6, 18, or 24 h (P < 0.001). Pretreatment with N. sativa (15.62–250 μg/ml) and TQ (1.17–37.5 μM) reduced SGD-induced cytotoxicity in PC12 cells after 6 and 18 h. A significant increase
in intracellular ROS production was seen following SGD (P < 0.001). N. sativa (250 μg/ml, P < 0.01) and TQ (2.34, 4.68, 9.37 μM, P < 0.01) pretreatment reversed the increased ROS production following ischemic insult. The experimental results suggest that
N. sativa extract and TQ protects the PC12 cells against SGD-induced cytotoxicity via antioxidant mechanisms. Our findings might raise
the possibility of potential therapeutic application of N. sativa extract and TQ for managing cerebral ischemic and neurodegenerative disorders. 相似文献
18.
Pereira RP Fachinetto R de Souza Prestes A Puntel RL Santos da Silva GN Heinzmann BM Boschetti TK Athayde ML Bürger ME Morel AF Morsch VM Rocha JB 《Neurochemical research》2009,34(5):973-983
Considering the important role of oxidative stress in the pathogenesis of several neurological diseases, and the growing evidence
of the presence of compounds with antioxidant properties in the plant extracts, the aim of the present study was to investigate
the antioxidant capacity of three plants used in Brazil to treat neurological disorders: Melissa officinalis, Matricaria recutita and Cymbopogon citratus. The antioxidant effect of phenolic compounds commonly found in plant extracts, namely, quercetin, gallic acid, quercitrin
and rutin was also examined for comparative purposes. Cerebral lipid peroxidation (assessed by TBARS) was induced by iron
sulfate (10 μM), sodium nitroprusside (5 μM) or 3-nitropropionic acid (2 mM). Free radical scavenger properties and the chemical
composition of plant extracts were assessed by 1′-1′ Diphenyl-2′ picrylhydrazyl (DPPH) method and by Thin Layer Chromatography
(TLC), respectively. M. officinalis aqueous extract caused the highest decrease in TBARS production induced by all tested pro-oxidants. In the DPPH assay, M. officinalis presented also the best antioxidant effect, but, in this case, the antioxidant potencies were similar for the aqueous, methanolic
and ethanolic extracts. Among the purified compounds, quercetin had the highest antioxidant activity followed by gallic acid,
quercitrin and rutin. In this work, we have demonstrated that the plant extracts could protect against oxidative damage induced
by various pro-oxidant agents that induce lipid peroxidation by different process. Thus, plant extracts could inhibit the
generation of early chemical reactive species that subsequently initiate lipid peroxidation or, alternatively, they could
block a common final pathway in the process of polyunsaturated fatty acids peroxidation. Our study indicates that M. officinalis could be considered an effective agent in the prevention of various neurological diseases associated with oxidative stress. 相似文献
19.
Naveen Kumar Kalagatur Elsayed Fathi Abd_Allah Sudhakar Poda Krishna Kadirvelu Abeer Hashem Venkataramana Mudili Chandranayaka Siddaiah 《Saudi Journal of Biological Sciences》2021,28(1):465-477
Deoxynivalenol (DON) is Fusarium mycotoxin that is frequently found in many cereal-based foods, and its ingestion has a deleterious impact on human health. In this investigation, we studied the mechanism of DON-induced neurotoxicity and followed by cytoprotective efficacy of quercetin (QUE) in contradiction of DON-induced neurotoxicity through assessing the oxidative stress and apoptotic demise in the human neuronal model, i.e. SH-SY5Y cells. DON diminished the proliferation of cells in the manner of dose and time-dependent as revealed by cell viability investigations, i.e. MTT and lactate dehydrogenase assays. Additional studies, such as intracellular reactive oxygen species (ROS), lipid peroxidation (LPO), mitochondrial membrane potential (MMP), DNA damage, cell cycle, and neuronal biomarkers (amino acid decarboxylase, tyrosine hydroxylase, and brain-derived neurotrophic factor) demonstrated that DON induces apoptotic demise in neuronal cells through oxidative stress intermediaries. On another hand, pre-treatment of neuronal cells with 1 mM of quercetin (QUE) showed decent viability upon exposure to 100 µM of DON. In detailed studies demonstrated that QUE (1 mM) pre-treated cells show strong attenuation efficiency against DON-induced ROS generation, LPO, MMP loss, DNA impairment, cell cycle arrest, and down-regulation of neuronal biomarkers. The consequences of the investigation concluded that QUE mitigates the DON-induced stress viz., decreased ROS production and LPO generation, upholding MMP and DNA integrity and regulation of neuronal biomarker gene expression in SH-SY5Y cells. 相似文献
20.
Oxidative stress is a damaging process resulting from an imbalance between excessive generation of oxidant compounds and insufficient
antioxidant defence mechanisms. Oxidative stress plays a crucial role in the initiation and progression of cigarette smoke-induced
lung injury, deterioration in lung functions, and development of chronic obstructive pulmonary disease (COPD). In smokers
and in patients with COPD, the increased oxidant burden derives from cigarette smoke per se, and from activated inflammatory cells releasing enhanced amounts of reactive oxygen and nitrogen species (ROS, RNS, respectively).
Although mild oxidative stress resulting from cigarette smoking leads to the upregulation of the antioxidative enzymes synthesis
in the lungs, high levels of ROS and RNS observed in patients with COPD overwhelm the antioxidant enzymes capacities, resulting
in oxidant-mediated lung injury and cell death. In addition, depletion of antioxidative systems in the systemic circulation
was consistently observed in such patients. The imbalance between the generation of ROS/RNS and antioxidant capacities — the
state of “oxidative stress” — is one of the major pathophysiologic hallmarks in the development of COPD. Detrimental effects
of oxidative stress include impairment of membrane functions, inactivation of membrane-bound receptors and enzymes, and increased
tissue permeability. In addition, oxidative stress aggravates the inflammatory processes in the lungs, and contributes to
the worsening of the protease-antiprotease imbalance. Several markers of oxidative stress, such as increases in lipid peroxidation
products and reductions in glutathione peroxidase activity, have been shown to be related to the reductions in pulmonary functions.
In the present article we review the current knowledge about the vicious cycle of cigarette smoking, oxidative stress, and
inflammation in the pathogenesis of COPD. 相似文献