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1.
Andrea Ferrigno Cesarina Gregotti Plinio Richelmi Mariapia Vairetti 《In vitro cellular & developmental biology. Animal》2010,46(5):445-449
In the present study, the effects of dexamethasone on cadmium-induced toxicity were evaluated in isolated rat hepatocytes.
Hepatocytes were cultured for 24 h in William’s E medium containing fetal calf serum (10%), insulin (0.1 IU/ml), and glucagon
(0.01 μM) in the absence or presence of 0.1 μM dexamethasone. Cadmium chloride, 5 or 10 μM, was added to the medium and the
toxicity was evaluated for up to 48 h after treatment. Lactate dehydrogenase (LDH) release, the reduced and oxidized glutathione
ratio (GSH/GSSG), protein-SH groups, and lipid peroxidation levels were evaluated. Cadmium induced a dose- and time-dependent
LDH release in control hepatocytes at 24 h (Cd 10 μM 42%) while hepatocytes pretreated with dexamethasone showed lower necrosis
(Cd 10 μM 12% at 24 h). GSH/GSSH ratio and protein-SH groups were higher while lipid peroxidation was lower in dexamethasone-treated
hepatocytes as compared with untreated cells. In conclusion, cadmium toxicity was associated with an increase in intracellular
oxidative stress responsible for accelerated cell death. The use of dexamethasone prevented cadmium damage, suggesting that
the cytoprotective action of this hormone is related to its effect in preventing changes in thiols such as glutathione and
protein-SH groups. 相似文献
2.
Greenhouse hydroponic experiments were conducted using Cd-sensitive (Xiushui63) and tolerant (Bing97252) rice genotypes to
evaluate genotypic differences in response of photosynthesis and phytochelatins to Cd toxicity in the presence of exogenous
glutathione (GSH). Plant height, chlorophyll content, net photosynthetic rate (Pn), and biomass decreased in 5 and 50 μM Cd
treatments, and Cd-sensitive genotype showed more severe reduction than the tolerant one. Cadmium stress caused decrease in
maximal photochemical efficiency of PSII (Fv/Fm) and effective PSII quantum yield [Y(II)] and increase in quantum yield of
regulated energy dissipation [Y(NPQ)], with changes in Cd-sensitive genotype being more evident. Cadmium-induced phytochelatins
(PCs), GSH, and cysteine accumulation was observed in roots of both genotypes, with markedly higher level in PCs and GSH on
day 5 in Bing97252 compared with that measured in Xiushui63. Exogenous GSH significantly alleviated growth inhibition in Xiushui63
under 5 μM Cd and in both genotypes in 50 μM Cd. External GSH significantly increased chlorophyll content, Pn, Fv/Fm, and
Y(II) of plants exposed to Cd, but decreased Y(NPQ) and the coefficient of non-photochemical quenching (qN). GSH addition
significantly increased root GSH content in plants under Cd exposure (except day 5 of 50 μM Cd) and induced up-regulation
in PCs of 5 μM-Cd-treated Bing97252 throughout the 15-day and Xiushui63 of 5-day exposure. The results suggest that genotypic
difference in the tolerance to Cd stress was positively linked to the capacity in elevation of GSH and PCs, and that alleviation
of Cd toxicity by GSH is related to significant improvement in chlorophyll content, photosynthetic performance, and root GSH
levels. 相似文献
3.
Diabetic neuropathy is one of the most frequent complications of diabetes. Despite some studies, the exact mechanism of glucose
neurotoxicity has not been fully elucidated. Increased reactive oxygen species (ROS) has proposed as a possible mechanism.
Crocus sativus L. (saffron) has been known as a source of antioxidants. Therefore, neuroprotective effect of saffron extract, its active
component crocin and γ-glutamylcysteinylglycine (GSH) was studied in glucose-induced neurotoxicity, using PC12 cells as a
suitable in vitro model of diabetic neuropathy. Cell viability was quantitated by MTT assay. ROS was measured using DCF-DA
by flow cytometry analysis. The result showed that glucose (13.5 and 27 mg/ml) reduced the cell viability of PC12 cells after
4 days. Saffron extract (5 and 25 mg/ml), crocin (10 and 50 μM) and GSH (10 μM) could decrease this toxicity. Glucose toxicity
was consistent with increased ROS production which reduced by saffron, crocin and GSH pretreatment. These results suggest
saffron and its carotenoid crocin could be potentially useful in diabetic neuropathy treatment. 相似文献
4.
Impact of cadmium in T lymphocyte subsets and cytokine expression: differential regulation by oxidative stress and apoptosis 总被引:3,自引:0,他引:3
Cadmium (Cd), a possible human carcinogen is a potent immunotoxicant. In rodents it causes thymic atrophy and splenomegaly,
in addition to immuno-suppression and modulation of humoral and/or cellular immune response. Oxidative stress and apoptosis
appear to be underlying mechanism of Cd induced thymic injury. To understand the involvement of reactive oxygen species (ROS),
intracellular glutathione (GSH) and apoptosis in modulation of T-cell repertoire, we studied the effect of Cd (10, 25 and
50 μM) on primary T lymphocytes of BALB/c mice at different time intervals (6, 12 and 18 h). We observed a dose and time dependent
decline in CD4+/CD8+ ratio (a bio-indicator of immunotoxicity) as a result of significant suppression of CD4+ subsets (helper T-cells) and enhancement in CD8+ cells (cytotoxic T-cells) At the same time, the CD4+CD8+ (DP) cell population was lowered while the CD4−CD8− (DN) cells were increased. The oxidative stress and apoptotic data revealed almost similar ROS generation in both CD4+ and CD8+ cells, but relatively more marked GSH depletion and apoptosis in CD4+ than in CD8+ population. On further analysis of CD4+ T-subsets, cytokine release (IL-2 and IFNγ) by Th 1 cells and IL-4 by Th 2 cells were shown to be significantly suppressed
in a dose responsive manner. The highest inhibition was observed in IFNγ, then IL-2 followed by IL-4. In conclusion, our data
demonstrates that T-cell apoptosis by Cd, more in CD4+ than in CD8+ cells appear related to higher depletion of intracellular glutathione. Th 1 cells of CD4+ sub-population are more responsive to Cd than Th 2, leading to higher suppression of IL-2 and IFNγ than IL-4 and hence, the
study unravels to some extend, the underlying events involved in Cd immunotoxicity. 相似文献
5.
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
6.
In this study, the effect of cadmium (Cd) on cell viability and its accumulation in Bradyrhizobium spp. (peanut microsymbionts) as well as the role of glutathione (GSH) in the tolerance to this metal were investigated. A
reference strain recommended as peanut inoculant (Bradyrhizobium sp. SEMIA6144) grew up to 10 μM Cd meanwhile a GSH-deficient mutant strain (Bradyrhizobium sp. SEMIA6144-S7Z) was unable to grow at this concentration. Two native peanut isolates obtained from Córdoba soils (Bradyrhizobium sp. NLH25 and Bradyrhizobium sp. NOD31) tolerated up to 30 μM Cd. The analysis of Cd content showed that Bradyrhizobium sp. SEMIA6144 accumulated a high amount of this metal, but a considerable inhibition of growth was observed compared to tolerant
strains at 10 μM Cd. At this concentration, the intracellular GSH content of all the Bradyrhizobium sp. strains was not modified in comparison to control conditions. However, at 30 μM Cd, the intracellular GSH content significantly
increased in Bradyrhizobium sp. strains NLH25 and NOD31. Thus, the distinct response of each Bradyrhizobium sp. strain to Cd reveals that, even in closely related lineages, there are strain-specific variations influencing the levels
of tolerance to this metal. Indeed, the native peanut isolates tolerated higher Cd concentration than the reference strain,
possibly due to an increase in GSH levels which could act as a detoxifying agent. 相似文献
7.
Cadmium (Cd) is a highly toxic metal that enters the food chain. Following oral ingestion, the intestinal epithelium is the
first biological barrier crossed by Cd and is also an important target tissue. In the present study, the human intestinal
Caco-2 cell line was used to evaluate the impact of a low level of exposure on both undifferentiated and differentiated intestinal
cells. As revealed by the LC50 values estimated with the 3-[4,5-dimethyl-2-thiazol-2-yl]-2,5-diphenyltetrazolium bromide (MTT) assay, mature Caco-2 cells
were more resistant to Cd. However, following a 24-h exposure to non-cytotoxic levels of Cd (10 μM) or zinc (Zn, 100 μM),
threefold increases were obtained in the LC50 values of 7-day-old cells, whereas increased resistance in 21-day-old cells was observed exclusively with Zn. Induction of
MT-IIa and HSP70 mRNAs was higher in undifferentiated cells and an increase in cellular glutathione (GSH) content was observed
exclusively in these cell cultures. However, the results obtained with cycloheximide used for inhibiting protein synthesis
and with l-buthionine sulfoximine (BSO), which inhibits GSH synthesis, revealed that protein synthesis is not a prerequisite to the
development of resistance. The presence of 100 mM 3-amino-1,2,4-triazole (3AT), a catalase inhibitor, prevented Cd-induced
but not Zn-induced resistance, as well as sensitized cells to Cd toxicity. These results show for the first time differences
in constitutive and acquired resistance to Cd as a function of enterocytic differentiation status and suggest the involvement
of different mechanisms for Cd- and Zn-induced adaptation in the intestinal cells. Redox signals may trigger Cd-induced adaptation
mechanisms but pro-oxidant conditions would eliminate proliferative intestinal cells capability to develop resistance. This
would be critical for Cd- but not Zn-induced mechanisms of resistance since Cd but not Zn may cause oxidative stress. 相似文献
8.
The role of glutathione (GSH) in the adaptation of wild type Arabidopsis thaliana plants to Cd stress was investigated. The nutrient solution (control or containing 50 or 100 μM Cd) was supplemented with
buthionine sulfoximine (BSO; 50, 100, 500 μM, to decrease the GSH content in plants) or GSH (50, 100, 500 μM, to increase
its content in plants) in order to find how GSH content could regulate Cd stress responses. BSO application did not influence
plant biomass, while exogenous GSH (especially 500 μM) reduced root biomass. BSO (500μM) in combination with Cd (100 μM) increased
Cd toxicity on root growth (by over 50 %), most probably due to reduced GSH content and phytochelatin (PC) accumulation (by
over 96 %). On the other hand, combination of exogenous GSH (500 μM) with Cd (100 μM) was also more toxic to plants than Cd
alone despite a significant increase in GSH and PC accumulation (up to 2.7 fold in the roots). This fact could indicate that
the natural content of endogenous GSH in wild type A. thaliana plants is sufficient for Cd-tolerance. A decrease in this GSH content led to decreased Cd-tolerance of the plants but an
increase in GSH content did not enhance Cd-tolerance, and it showed even toxic effect on the plants. 相似文献
9.
Cadmium (Cd) homeostasis and detoxification in sunflower (Helianthus annuus L.) cells differing in Cd sensitivity/tolerance were studied by analyzing the glutathione-mediated antioxidant mechanism
vis-à-vis phytochelatin biosynthesis in vitro. Calluses exposed to Cd-shock/-acclimatization (150μM) were assayed for oxidative stress, reduced glutathione (GSH), glutathione
disulfide (GSSG), phytochelatins (PCs) and reactive oxygen species (ROS). Although Cd did not induce any oxidative stress
in Cd-tolerant callus (TCd), it generated oxidative stress in Cd-shock callus (SCd) both in terms of lipid peroxidation and
protein oxidation. GSH/GSSG ratio remained similar to control values in the cadmium-acclimatized calluses. However, after
acute treatment, there was a decline in both GSH and GSSG levels in SCd with concomitant reduction in the GSH/GSSG ratio.
Analysis of PCs was performed using HPLC and mass spectrometry methods. PC concentration in TCd were approximately twice those
that in SCd, showing in both cases a 1:2:1 relative proportion for PC n = 2 (PC2): PC n = 3 (PC3): PC n = 4 (PC4). Calluses growing in the presence of Cd developed an increased resistance to paraquat oxidative stress generation.
These results indicated that PCs synthesis was an important mechanism for Cd detoxification in sunflower calluses, but the
capacity to grow in the presence of Cd is related to the tissues ability to maintain high intracellular levels of GSH. 相似文献
10.
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
11.
Today cardiovascular diseases (CVDs) are the killer number one world wide. In 2004 an estimated 17.1 million people died due
to CVDs and this number will further increase to an estimated 23.6 million by 2030. Importantly, currently known risk factors,
like hypertension, and hypercholesterolemia, can only be made responsible for about 50–75% of all CVDs, highlighting the urgent
need to search for and define new CVD risk factors. Cadmium (Cd) was shown to have the potential to serve as one such novel
risk factor, as it was demonstrated—in vitro, in animal studies, and in human studies—that Cd causes atherosclerosis (the
basis of most CVDs). Herein, we discuss the molecular and cellular biological effects of Cd in the cardiovascular system;
we present concepts on the pathophysiology of Cd-caused atherosclerosis, and provide data that indicate an epidemiological
relevance of Cd as a risk factor for CVDs. 相似文献
12.
In a pot-soil culture ameliorative effect of sulphur (S) (0 or 40 mg S kg−1 soil) on cadmium (Cd) (0, 25, 50 and 100 mg Cd kg−1 soil)-induced growth inhibition and oxidative stress in mustard (Brassica campestris L.) cultivar Pusa Gold was studied. Cadmium at 100 mg kg−1 soil caused maximum increase in the contents of Cd and thiobarbituric acid reactive substances (TBARS) in leaves. Maximum
reductions in growth (plant dry mass, leaf area), chlorophyll content, net photosynthetic rate (PN) and the contents of ascorbate (AsA), glutathione (GSH) were observed with 100 mg Cd kg−1 soil compared to control. The application of S helped in reducing Cd toxicity, which was greater for 25 and 50 mg Cd kg−1 soil) compared to 100 mg Cd kg−1 soil. Addition of S to Cd-treated plants showed decrease in Cd and TBARS content in leaves and restoration of growth and
photosynthesis through increase in the contents of AsA and GSH. Net photosynthetic rate and plant dry mass were strongly and
positively correlated with the contents of AsA and GSH. It is suggested that S may ameliorate Cd toxicity and protects growth
and photosynthesis of mustard involving AsA and GSH. 相似文献
13.
Savita Gangwar Vijay Pratap Singh Sheo Mohan Prasad Jagat Narayan Maurya 《Acta Physiologiae Plantarum》2011,33(2):451-462
Present study showed the responses of pea seedlings to exogenous indole acetic acid (IAA; 10 and 100 μM) application under
manganese (Mn; 50, 100 and 250 μM) toxicity. Manganese and 100 μM IAA alone as well as in combination decreased growth of
pea seedlings compared to control. Moreover, some parameters of oxidative stress—hydrogen peroxide (H2O2) and malondialdehyde (MDA) were also increased by single and combined treatments of Mn and 100 μM IAA compared to control.
In contrast, addition of 10 μM IAA together with Mn, alleviated Mn toxicity symptoms and promoted growth led to the decrease
in H2O2 and MDA levels compared to Mn treatments alone. Under single and combined treatments of Mn and 100 μM IAA, catalase activity
decreased while superoxide dismutase and ascorbate peroxidase activities increased and glutathione reductase and dehydroascorbate
reductase exhibited differential responses. However, addition of 10 μM IAA together with Mn, increased activities of studied
enzymatic antioxidants. Root and shoot reduced ascorbate (AA) and reduced glutathione (GSH) and, their reduced/oxidized ratios
decreased while dehydroascorbate (DHA) and oxidized glutathione (GSSG) contents increased compared to control following single
and combined treatments of Mn and 100 μM IAA. However, supply of 10 μM IAA together with Mn, increased AA and GSH, and their
reduced/oxidized ratios in root and shoot compared to Mn treatments alone. This study thus suggests that 10 μM of IAA was
able to increase Mn tolerance in pea seedlings under Mn toxicity while opposite was noticed for 100 μM IAA. 相似文献
14.
The increasing applications of silicon dioxide (SiO2) nanomaterials have been widely concerned over their biological effects and potential hazard to human health. In this study,
we explored the effects of SiO2 nanoparticles (15, 30, and 100 nm) and their micro-sized counterpart on cultured human epidermal Keratinocyte (HaCaT) cells.
Cell viability, cell morphology, reactive oxygen species (ROS), DNA damage (8-OHdG, γH2AX and comet assay) and apoptosis were
assessed under control and SiO2 nanoparticles exposed conditions. As observed in the Cell Counting Kit-8 (CCK-8) assay, exposure to 15, 30 or 100 nm SiO2 nanoparticles at dosage levels between 0 and 100 μg/ml decreased cell viability in a concentration- and size dependent manner
and the IC50 of 24 hour exposure was 19.4 ± 1.3, 27.7 ± 1.5 and 35.9 ± 1.6 μg/ml for 15, 30 and 100 nm SiO2 nanoparticles, respectively. Morphological examination revealed cell shrinkage and cell wall missing after SiO2 nanoparticle exposure. Increase in intracellular ROS level and DNA damage as well as apoptosis were also observed in SiO2 nanoparticle-exposed HaCaT cells. Exposure to SiO2 nanoparticles results in a concentration- and size-dependent cytotoxicity and DNA damage in cultural HaCaT cells which is
closely correlated to increased oxidative stress. 相似文献
15.
Hyperactivation of the hypothalamic–pituitary–adrenal axis and the associated hippocampal atrophy were observed in patients
with depression, which could be ameliorated by the treatment with antidepressants. Therefore, neuroprotection has been proposed
to be one of the acting mechanisms of antidepressant. Our previous studies have showed that treating mice with piperine produced
antidepressant-like effect in animal models of behavioral despair. This study aimed to examine the protective effect of piperine
treatment on corticosterone-induced neurotoxicity in cultured rat pheochromocytoma (PC12) cells. The results showed that piperine
co-treatment revealed a differential effect on the cytotoxicity of corticosterone and had its maximum inhibitory effect at
1 μM. Piperine (1 μM) co-treatment also significantly decreased intracellular reactive oxygen species level, and enhanced
superoxide dismutase activity and total glutathione level in corticosterone-treated PC12 cells. In addition, piperine (1 μM)
co-treatment was found to reverse the decreased brain-derived neurotrophic factor (BDNF) mRNA level caused by corticosterone
in PC12 cells. The results suggest that piperine exerts a neuroprotective effect on corticosterone-induced neurotoxicity in
PC12 cells, at least in part, via the inhibition of oxidative stress and the upregulation of BDNF mRNA expression. This neuroprotective
effect may be one of the acting mechanisms accounts for the in vivo antidepressant activity of piperine. 相似文献
16.
To understand how plants from the Fabaceae family maintain zinc (Zn) homeostasis, we have characterized the kinetics of three
Zn transporting proteins from the ZIP family of divalent metal transporters in the model legume Medicago truncatula. Of six ZIP’s studied, MtZIP1, MtZIP5 and MtZIP6 were the only members from this family determined to transport Zn and were
further characterized. MtZIP1 has a low affinity for Zn with a Km of 1 μM as compared to MtZIP5 and MtZIP6 that have a higher affinity for Zn with Km of 0.4 μM and 0.3 μM, respectively. Zn transport by MtZIP1 was more sensitive to inhibition by copper (Cu) concentrations
than MtZIP5 and MtZIP6, because 3 μM Cu inhibited Zn transport by 80% in MtZIP1 while 5 μM Cu was required to achieve the
same inhibition of Zn transport in MtZIP5 and MtZIP6. Cadmium (Cd) had a greater effect on the ability of MtZIP1 to transport
Zn than MtZIP5 and MtZIP6, because at a concentration of 3 μM Cd, the Zn transport by MtZIP1 was inhibited 55% and the transport
of Zn by MtZIP5 and MtZIP6 was inhibited by 20–30%. However, only MtZIP6 transported Cd at higher rates than those observed
in the control plasmid pFL61, demonstrating a low affinity for Cd based on a Km of 57 μM. These results suggest that Medicago truncatula has both high and low affinity Zn transporters to maintain Zn homeostasis and that these transporters may function in different
compartments within the plant. 相似文献
17.
Mercury (Hg) is an occupational and environmental contaminant that is a well-recognized health hazard. To approach the concrete
mechanisms of mercury nephrotoxicity and find out a new way to prevent it, the rats were subcutaneously injected with different
dosages of mercuric chloride (HgCl2)—0, 2.2, 4.4, and 8.8 μmol/kg. The levels of Hg, blood urea nitrogen (BUN), urine protein, glutathione (GSH), malondialdehyde
(MDA) and activities of N-acetyl-beta-d-glucosaminidase (NAG), alkaline phosphatase (ALP), lactate dehydrogenase (LDH), superoxide dismutase (SOD), and glutathione
peroxidase (GSH-Px) were investigated, and the levels of reactive oxygen species (ROS) and apoptosis and the pathological
changes were also observed. In addition, the effects of 1 mmol/kg tea polyphenols (TP) and 0.04 mmol/kg schisandrin B (Sch
B) were studied at 8.8 μmol/kg HgCl2. It was observed that the levels of Hg, BUN, urine protein, GSH, and MDA and activities of NAG, ALP, and LDH increased significantly;
the activities of SOD and GSH-Px decreased significantly; the levels of ROS and apoptosis increased obviously; and many pathological
changes occurred dose-dependently in the HgCl2 injection groups. Further investigation indicated that pretreatment with TP and Sch B significantly reversed the toxic effects
of HgCl2. These results suggested that TP and Sch B might antagonize the nephrotoxicity caused by HgCl2 exposure. 相似文献
18.
Cadmium-induced oxidative damage and antioxidative defense mechanisms in <Emphasis Type="Italic">Vigna mungo</Emphasis> L. 总被引:1,自引:1,他引:0
Alicia S. Molina Carlos Nievas María Verónica Pérez Chaca Francisco Garibotto Ulises González Silvana M. Marsá Celina Luna María Sofía Giménez Fanny Zirulnik 《Plant Growth Regulation》2008,56(3):285-295
Cadmium (Cd)-induced oxidative stress and antioxidant defense mechanisms were analyzed in roots and leaves of Vigna mungo L. Seeds were germinated in perlite-vermiculite and irrigated with Hoagland nutrient solution. At day 6, seedlings were exposed
to 40 μM Cd under semi-hydroponic conditions for a period of 12 days. Growth anomalies and abnormal chromatin condensation
were observed in Cd-treated plants, in comparison with control ones. Cd accumulation was observed in roots of treated plants.
The analyses of antioxidative defense and oxidative parameters in roots, stems and leaves showed different tissue-specific
responses. Superoxide dismutase (SOD) and guaiacol peroxidase (GPx) activities and the level of lipid peroxidation (MDA content)
decreased in roots. However, they increased in leaves. Catalase activity and chlorophyll content, on the other hand, decreased
over exposure to Cd stress. Total glutathione, non-protein thiols, reduced glutathione (GSH) and phytochelatins increased
significantly, while oxidized glutathione (GSSG) decreased, as compared with control plants. The present data suggest that
the presence of Cd in soil and water can cause oxidative damage that may be detrimental for optimum production of nutritional
mung. 相似文献
19.
The effect of noncytotoxic doses of argemone oil (AO) and butter yellow (BY), the common adulterants in edible oil, on free
radical generation and signaling pathway for cell proliferation in primary cells of gall bladder (GB) was undertaken. AO and
BY showed no cytotoxicity at 0.1 μl/ml and 0.1 μg/ml concentration, respectively. AO caused significant increase in ROS after
30 min and RNS after 24 h in GB cells while no change was observed following BY treatment. Enhanced level of COX-2 was observed
following AO (0.1 μl/ml) and BY (0.1 μg/ml) treatment to cells for 24 h. AO treatment caused phosphorylation of ErbB2, AKT,
ERK, and JNK along with increased thymidine uptake indicating cell proliferation ability in GB cells. BY treatment also showed
significant expression of these proteins with the exception of phosphorylated JNK. These results suggest that AO and BY have
cell proliferative potential in GB cells following up-regulation of COX-2 and ErbB2; however, their downstream signaling molecules
and free radical generation have differential response, indicating that the mechanism of proliferation is different for both
compounds and may have relevance in gall bladder cancer. 相似文献
20.
Spice active principles as the inhibitors of human platelet aggregation and thromboxane biosynthesis
R.H. Raghavendra K. Akhilender Naidu 《Prostaglandins, leukotrienes, and essential fatty acids》2009,81(1):73-78
Spice active principles are reported to have anti-diabetic, anti-hypercholesterolemic, antilithogenic, anti-inflammatory, anti-microbial and anti-cancer properties. In our previous report we have shown that spices and their active principles inhibit 5-lipoxygenase and also formation of leukotriene C4. In this study, we report the modulatory effect of spice active principles viz., eugenol, capsaicin, piperine, quercetin, curcumin, cinnamaldehyde and allyl sulphide on in vitro human platelet aggregation. We have demonstrated that spice active principles inhibit platelet aggregation induced by different agonists, namely ADP (50 μM), collagen (500 μg/ml), arachidonic acid (AA) (1.0 mM) and calcium ionophore A-23187 (20 μM). Spice active principles showed preferential inhibition of arachidonic acid-induced platelet aggregation compared to other agonists. Among the spice active principles tested, eugenol and capsaicin are found to be most potent inhibitors of AA-induced platelet aggregation with IC50 values of 0.5 and 14.6 μM, respectively. The order of potency of spice principles in inhibiting AA-induced platelet aggregation is eugenol>capsaicin>curcumin>cinnamaldehyde>piperine>allyl sulphide>quercetin. Eugenol is found to be 29-fold more potent than aspirin in inhibiting AA-induced human platelet aggregation. Eugenol and capsaicin inhibited thromboxane B2 (TXB2) formation in platelets in a dose-dependent manner challenged with AA apparently by the inhibition of the cyclooxygenase (COX-1). Eugenol-mediated inhibition of platelet aggregation is further confirmed by dose-dependent decrease in malondialdehyde (MDA) in platelets. Further, eugenol and capsaicin inhibited platelet aggregation induced by agonists—collagen, ADP and calcium ionophore but to a lesser degree compared to AA. These results clearly suggest that spice principles have beneficial effects in modulating human platelet aggregation. 相似文献