共查询到20条相似文献,搜索用时 109 毫秒
1.
Eva Tvrd Daniel Lovíek Stanislav Kyzek Duan Kov
ik Elika Glov 《International journal of molecular sciences》2021,22(9)
Significant antibacterial properties of non-thermal plasma (NTP) have converted this technology into a promising alternative to the widespread use of antibiotics in assisted reproduction. As substantial data available on the specific in vitro effects of NTP on male reproductive cells are currently missing, this study was designed to investigate selected quality parameters of human spermatozoa (n = 51) exposed to diffuse coplanar surface barrier discharge NTP for 0 s, 15 s, 30 s, 60 s and 90 s. Sperm motility characteristics, membrane integrity, mitochondrial activity, production of reactive oxygen species (ROS), DNA fragmentation and lipid peroxidation (LPO) were investigated immediately following exposure to NTP and 2 h post-NTP treatment. Exposure to NTP with a power input of 40 W for 15 s or 30 s was found to have no negative effects on the sperm structure or function. However, a prolonged NTP treatment impaired all the sperm quality markers in a time- and dose-dependent manner. The most likely mechanism of action of high NTP doses may be connected to ROS overproduction, leading to plasma membrane destabilization, LPO, mitochondrial failure and a subsequent loss of motility as well as DNA integrity. As such, our findings indicate that appropriate plasma exposure conditions need to be carefully selected in order to preserve the sperm vitality, should NTP be used in the practical management of bacteriospermia in the future. 相似文献
2.
Punicalagin (PU) is a known antioxidant. The present study examined PU to protect against lead-induced oxidative stress (OS) testicular damage in mice. Significant increase in lipid peroxidation (LPO) after intraperitoneal injection of lead acetate (LA) indicated enormous generation of reactive oxygen species (ROS). Lead-induced OS has a direct effect on the differentiation of spermatogonial cells, showing a significant decline in sperm count. Supplementation of PU significantly changes values of LPO and glutathione (GSH) with a concomitant increase in sperm count, a marked decrease in the abnormal sperms, and a decline in the morphologically abnormal sperm population. Moreover, the histopathological evaluation of testes and epididymides showed severe changes in mice treated with LA. PU significantly induced nuclear factor erythroid-2 related factor 2-like 2 (Nrf2) expression and phase II enzymes, and data suggest that PU may inhibit OS through Nrf2 activation. The fertility test proved that PU might play an important role in male infertility treatment, especially in the type of infertility induced by OS. 相似文献
3.
Pavel Rossner Jr. Simona Strapacova Jitka Stolcpartova Jana Schmuczerova Alena Milcova Jiri Neca Veronika Vlkova Tana Brzicova Miroslav Machala Jan Topinka 《International journal of molecular sciences》2016,17(9)
We investigated the toxicity of benzo[a]pyrene (B[a]P), 1-nitropyrene (1-NP) and 3-nitrobenzanthrone (3-NBA) in A549 cells. Cells were treated for 4 h and 24 h with: B[a]P (0.1 and 1 μM), 1-NP (1 and 10 μM) and 3-NBA (0.5 and 5 μM). Bulky DNA adducts, lipid peroxidation, DNA and protein oxidation and mRNA expression of CYP1A1, CYP1B1, NQO1, POR, AKR1C2 and COX2 were analyzed. Bulky DNA adducts were induced after both treatment periods; the effect of 1-NP was weak. 3-NBA induced high levels of bulky DNA adducts even after 4-h treatment, suggesting rapid metabolic activation. Oxidative DNA damage was not affected. 1-NP caused protein oxidation and weak induction of lipid peroxidation after 4-h incubation. 3-NBA induced lipid peroxidation after 24-h treatment. Unlike B[a]P, induction of the aryl hydrocarbon receptor, measured as mRNA expression levels of CYP1A1 and CYP1B1, was low after treatment with polycyclic aromatic hydrocarbon (PAH) nitro-derivatives. All test compounds induced mRNA expression of NQO1, POR, and AKR1C2 after 24-h treatment. AKR1C2 expression indicates involvement of processes associated with reactive oxygen species generation. This was supported further by COX2 expression induced by 24-h treatment with 1-NP. In summary, 3-NBA was the most potent genotoxicant, whereas 1-NP exhibited the strongest oxidative properties. 相似文献
4.
F. B. Pruijn G. R. M. M. Haenen A. Bast 《European Journal of Lipid Science and Technology》1991,93(6):216-221
Free radicals can disturb the intracellular homeostasis by either modification of essential free sulfhydryl groups or by inducing lipid peroxidation. The damage provoked by oxidation of sulfhydryl groups might be reversible but the damage induced by the process of lipid peroxidation is probably not reversible. The main protective constituents of the cell are thiols and vitamin E. Thiols, especially glutathione, protect the cytosol while vitamin E protects the lipid membranes against free radicals. In the scavenging of free radicals in the lipid membrane, vitamin E becomes oxidized. However continuous recycling of vitamin E by a reductase, with the cytosolic thiol glutathione as cofactor, will keep the vitamin E levels high enough to protect against lipid peroxidation. In the recycling glutathione is oxidized. Dihydrolipoic acid cannot provide directly reducing equivalents for the recycling of vitamin E by the free radical reductase. However indirectly, via the reduction of oxidized glutathione, dihydrolipoic acid can mediate the regeneration of vitamin E. One of the secondary mechanisms that mediates free radical induced damage is the rise in intracellular free Ca2+-concentration caused by inactivation of the endoplasmic reticulum ca2+-ATPase. The Ca2+-ATPase can be inactivated either by sulfhydryl alkylation or by lipid peroxidation. The authors used the thiol-alkylating agent N-ethylmaleimide, cystamine and ebselen. Dithiothreitol reversed the inhibition caused by all the three agents, while dihydrolipoic acid reversed the inhibition caused by ebselen. Glutathione was not able to reverse the effects of the sulfhydryl reactive agents. The reactivation of the microsomal Ca2+-ATPase by dihydrolipoic acid, may – besides the reduction of oxidized glutathione – contribute to the protective effect of dihydrolipoic acid on lipid peroxidation. 相似文献
5.
Qaisra Naheed Choudhry Mi Jeong Kim Tae Gyun Kim Jeong Hoon Pan Jun Ho Kim Sung Jin Park Jin Hyup Lee Young Jun Kim 《International journal of molecular sciences》2016,17(9)
Our work aimed to investigate the protective effects of saponin-based nanoemulsions of vitamin A and E against oxidative stress-induced cellular damage in AML-12 cells. Saponin nanoemulsions of vitamin A (SAN) and vitamin E (SEN) were prepared by high-pressure homogenization and characterized in terms of size, zeta potential, and polydispersity index. SEN and SAN protect AML-12 cells against oxidative stress-induced cellular damage more efficiently via scavenging reactive oxygen species (ROS), and reducing DNA damage, protein carbonylation, and lipid peroxidation. These results provide valuable information for the development of nanoemulsion-based delivery systems that would improve the antioxidant properties of vitamin A and E. 相似文献
6.
Brain regional oxidative damage is thought to be a central mechanism in the pathogenesis of Alzheimer’s disease (AD). Recent
studies of cerebrospinal fluid (CSF) have suggested that increased lipid peroxidation of CSF and CSF lipoproteins also may
occur in AD patients. In the present study, we determined the susceptibility of human CSF to ex vivo lipid peroxidation and tested the hypothesis that oxidized CSF lipoproteins may be neurotoxic. Whole CSF or a CSF lipoprotein
fraction (d<1.210 g/mL) was oxidized with 2,2′-azobis(2-amidino-propane)dihydrochloride (AAPH), a hydrophilic free-radical generator.
Kinetics of CSF lipid peroxidation were followed by a standard fluorescence product accumulation assay. Oxidation of AD CSF
yielded significantly shorter fluorescent lag times than controls, indicating reduced antioxidant capacity. Electrophoretic
mobilities of CSF apolipoproteins were specifically reduced upon oxidation of CSF with AAPH, suggesting that lipoproteins
are primary targets of CSF lipid peroxidation. Cultured neuronal cells were exposed to physiological concentrations of isolated
CSF lipoproteins oxidized with increasing concentrations of AAPH; the resulting neurotoxicity showed a significant linear
AAPH concentration-response relationship. These results suggest that oxidized CSF lipoproteins may contribute to the pathogenesis
of neurodegeneration in AD. 相似文献
7.
Seok Jong Song Su-mi Kim Sang-ho Lee Ju-Young Moon Hyeon Seok Hwang Jin Sug Kim Seon-Hwa Park Kyung Hwan Jeong Yang Gyun Kim 《International journal of molecular sciences》2020,21(22)
Introduction: A recent study showed that early renal tubular injury is ameliorated in Nod-like receptor pyrin domain-containing protein 3 (NLRP3) KO mice with rhabdomyolysis-induced acute kidney injury (RIAKI). However, the precise mechanism has not been determined. Therefore, we investigated the role of NLRP3 in renal tubular cells in RIAKI. Methods: Glycerol-mediated RIAKI was induced in NLRP3 KO and wild-type (WT) mice. The mice were euthanized 24 h after glycerol injection, and both kidneys and plasma were collected. HKC-8 cells were treated with ferrous myoglobin to mimic a rhabdomyolytic environment. Results: Glycerol injection led to increase serum creatinine, aspartate aminotransferase (AST), and renal kidney injury molecule-1 (KIM-1) level; renal tubular necrosis; and apoptosis. Renal injury was attenuated in NLRP3 KO mice, while muscle damage and renal neutrophil recruitment did not differ between NLRP3 KO mice and WT mice. Following glycerin injection, increases in cleaved caspase-3, poly (ADP-ribose) polymerase (PARP), and a decrease in the glutathione peroxidase 4 (GPX-4) level were observed in the kidneys of mice with RIAKI, and these changes were alleviated in the kidneys of NLRP3 KO mice. NLRP3 was upregulated, and cell viability was suppressed in HKC-8 cells treated with ferrous myoglobin. Myoglobin-induced apoptosis and lipid peroxidation were significantly decreased in siNLRP3-treated HKC-8 cells compared to ferrous myoglobin-treated HKC-8 cells. Myoglobin reduced the mitochondrial membrane potential and increased mitochondrial fission and reactive oxygen species (ROS) and lipid peroxidation levels, which were restored to normal levels in NLRP3-depleted HKC-8 cells. Conclusions: NLRP3 depletion ameliorated renal tubular injury in a murine glycerol-induced acute kidney injury (AKI) model. A lack of NLRP3 improved tubular cell viability via attenuation of myoglobin-induced mitochondrial injury and lipid peroxidation, which might be the critical factor in protecting the kidney. 相似文献
8.
Sandra Recuero Ariadna Delgado-Bermúdez Yentel Mateo-Otero Estela Garcia-Bonavila Marc Llavanera Marc Yeste 《International journal of molecular sciences》2021,22(19)
Parkinson disease protein 7 (PARK7) is a multifunctional protein known to be involved in the regulation of sperm motility, mitochondrial function, and oxidative stress response in mammalian sperm. While ROS generation is needed to activate the downstream signaling pathways required for sperm to undergo capacitation, oxidative stress has detrimental effects for sperm cells and a precise balance between ROS levels and antioxidant activity is needed. Considering the putative antioxidant role of PARK7, the present work sought to determine whether this protein is related to the sperm ability to withstand in vitro capacitation. To this end, and using the pig as a model, semen samples were incubated in capacitation medium for 300 min; the acrosomal exocytosis was triggered by the addition of progesterone after 240 min of incubation. At each relevant time point (0, 120, 240, 250, and 300 min), sperm motility, acrosome and plasma membrane integrity, membrane lipid disorder, mitochondrial membrane potential, intracellular calcium and ROS were evaluated. In addition, localization and protein levels of PARK7 were also assessed through immunofluorescence and immunoblotting. Based on the relative content of PARK7, two groups of samples were set. As early as 120 min of incubation, sperm samples with larger PARK7 content showed higher percentages of viable and acrosome-intact sperm, lipid disorder and superoxide levels, and lower intracellular calcium levels when compared to sperm samples with lower PARK7. These data suggest that PARK7 could play a role in preventing sperm from undergoing premature capacitation, maintaining sperm viability and providing a better ability to keep ROS homeostasis, which is needed to elicit sperm capacitation. Further studies are required to elucidate the antioxidant properties of PARK7 during in vitro capacitation and acrosomal exocytosis of mammalian sperm, and the relationship between PARK7 and sperm motility. 相似文献
9.
In an ongoing study, rat and human urine have been examined for the presence of malondialdehyde (MDA) derivatives as indicators
of the nature of lipid peroxidative damage caused by this compoundin vivo. MDA in urine was found to be present mainly in the form of two lysine adducts, one acetylated and the other unacetylated,
reflectingin vivo reactions with tissue proteins. Two minor metabolites were identified as adducts with the phospholipid bases serine and ethanolamine
and a third one as an adduct with the nucleic acid base guanine. The identification of an MDA adduct with deoxyguanosine (dG-MDA)
among the products of hydrolysis of rat liver DNA suggested the possible occurrence of this compound in urine. In the present
study dG-MDA was identified in rat and in human urine, and a high-performance liquid chromatographic method utilizing fluorescence
detection was developed for its estimation. The method is sensitive to 1 pmol of dG-MDA and requires a minimum of 1 mL of
rat urine or 5 mL of human urine. Its rate of excretion by five-week-old rats (28.54±2.28 nmol/kg/24 h) (mean±SEM) was higher
than that for nine-week-old rats (6.29±1.02) and much higher than that for adult humans (0.40±0.05). The results indicate
that, as reported for 8-hydroxy-deoxyguanosine, dG-MDA excretion is related to metabolic rate. Excretion of dG-MDA by the
rat, like the excretion of total MDA, declines during growth on a body weight basis at a rate similar to the decrease in resting
energy metabolism. In contrast to other MDA derivatives excreted in rat urine, vitamin E deficiency had no effect on the excretion
of dG-MDA. Together with evidence that the dG-MDA content of rat liver DNA likewise is unaffected by vitamin E depletion or
by administration of catalysts ofin vivo lipid peroxidation, these findings indicate that DNA is protected from lipid peroxidative damage, possibly through conservation
of the vitamin E associated with the lipids of the nuclear membrane. 相似文献
10.
Ken Ando Kunihide Nagata Masatoshi Beppu Kiyomi Kikugawa Terue Kawabata Kyoko Hasegawa Masao Suzuki 《Lipids》1998,33(5):505-512
Human erythrocytes in the circulation undergo dynamic oxidative damage involving membrane lipid peroxidation and protein aggregation
during aging. The present study was undertaken to determine the effect of n−3 fatty acid supplementation on lipid peroxidation
and protein aggregation in the circulation and also the in vitro susceptibility of rat erythrocyte membranes to oxidative damage. Wistar male rats were fed a diet containing n−6 fatty acid-rich
safflower oil or n−3 fatty acid-rich fish oil with an equal amount of vitamin E for 6 wk. n−3 Fatty acid content in erythrocyte
membranes of rats fed fish oil was significantly higher than that of rats fed safflower oil. The degree of membrane lipid
peroxidation and protein aggregation of rats fed fish oil was not significantly higher than that of rats fed safflower oil
when the amounts of phospholipid hydroper-oxides, thiobarbituric acid-reactive substances, and detergent-insoluble protein
aggregates were measured. When isolated erythrocytes were oxidized under aerobic conditions in the presence of Fe(III), the
degree of membrane lipid peroxidation of erythrocytes from rats fed fish oil was increased to a greater extent than that of
rats fed safflower oil, whereas the degree of membrane protein aggregation of both groups was increased in a similar extent.
Hence, n−3 fatty acid supplementation did not affect lipid peroxidation and protein aggregation in membranes of circulating
rat erythrocytes, and the supplementation increased the susceptibility of isolated erythrocytes to lipid peroxidation, but
not to protein aggregation, under the aerobic conditions. If a sufficient amount of vitamin E is supplied, n−3 fatty acid
supplementation may give no undesirable oxidative effects on rat erythrocytes in the circulation. 相似文献
11.
Ken Donaldson Fiona A Murphy Rodger Duffin Craig A Poland 《Particle and fibre toxicology》2010,7(1):1-17
Background
Increasing environmental and occupational exposures to nanoparticles (NPs) warrant deeper insight into the toxicological mechanisms induced by these materials. The present study was designed to characterize the cell death induced by carbon black (CB) and titanium dioxide (TiO2) NPs in bronchial epithelial cells (16HBE14o- cell line and primary cells) and to investigate the implicated molecular pathways.Results
Detailed time course studies revealed that both CB (13 nm) and TiO2(15 nm) NP exposed cells exhibit typical morphological (decreased cell size, membrane blebbing, peripheral chromatin condensation, apoptotic body formation) and biochemical (caspase activation and DNA fragmentation) features of apoptotic cell death. A decrease in mitochondrial membrane potential, activation of Bax and release of cytochrome c from mitochondria were only observed in case of CB NPs whereas lipid peroxidation, lysosomal membrane destabilization and cathepsin B release were observed during the apoptotic process induced by TiO2 NPs. Furthermore, ROS production was observed after exposure to CB and TiO2 but hydrogen peroxide (H2O2) production was only involved in apoptosis induction by CB NPs.Conclusions
Both CB and TiO2 NPs induce apoptotic cell death in bronchial epithelial cells. CB NPs induce apoptosis by a ROS dependent mitochondrial pathway whereas TiO2 NPs induce cell death through lysosomal membrane destabilization and lipid peroxidation. Although the final outcome is similar (apoptosis), the molecular pathways activated by NPs differ depending upon the chemical nature of the NPs. 相似文献12.
Although malondialdehyde (MDA) is extensively metabolized to CO2, small amounts are nevertheless excreted in an acid-hydrolyzable form in rat urine. In this study, urinary MDA was evaluated
as an indicator of lipid peroxidation in the diet and in the tissues. MDA was released from its bound form(s) in urine by
acid treatment and determined as the TBA-MA derivative by HPLC. MDA excretion by the rat was found to be responsive to oral
administration of the Na enol salt and to peroxidation of dietary lipids. Urinary MDA also increased in response to the increased
lipid peroxidation in vivo produced by vitamin E deficiency and by administration of iron nitrilotriacetate. Chronic feeding
of a diet containing cod liver oil led to increases in MDA excretion which were not completely eliminated by fasting or feeding
a peroxide-free diet, indicating that there was increased lipid peroxidation in vivo. MDA excretion was not responsive to
Se deficiency or CCl4 administration. DPPD, a biologically active antioxidant, but not BHA, a non-biologically active antioxidant, prevented the
increase in MDA excretion in vitamin E deficient animals. The results indicate that MDA excretion can serve as an indicator
of the extent of lipid peroxidation in the diet and, under conditions which preclude a dietary effect, as an index of lipid
peroxidation in vivo.
Part of this research was performed in fulfillment of the requirements for the MSc degree in nutrition. 相似文献
13.
l-3,4-Dihydroxyphenylalanine (l-dopa) is one of the few allelochemicals in which the phytotoxic action mechanism has been studied. Excess exogenous l-dopa suppresses root elongation in some plant species, and the inhibitory action is species-selective. The main factor of
phytotoxicity of l-dopa is considered to be oxidative damage by reactive oxygen species (ROS) and/or free radical species (FRS). This study
was performed to elucidate the mechanism of species-selective phytotoxicity. The involvement of ROS/FRS and polyphenol oxidase
(PPO) in species-selective phytotoxicity was examined with barnyardgrass (Echinochloa crus-galli L.) and lettuce (Lactuca sativa L.), tolerant and susceptible species, respectively. Lipid peroxidation and melanin accumulation correlated with growth inhibition
by L-dopa. Antioxidants, ascorbic acid and α-tocopherol, decreased lipid peroxidation and melanin accumulation and rescued
lettuce root from growth inhibition. The oxidation of L-dopa by PPO was much greater in lettuce than in barnyardgrass. From
these results, the phytotoxicity of L-dopa is considered due to the oxidative damage caused by ROS/FRS generated from the
melanin synthesis pathway. PPO activity might be involved in the mechanism of species-selective phytotoxicity between barnyardgrass
and lettuce. 相似文献
14.
Cerebral spinal fluid (CSF) lipoproteins have become a focus of research since the observation that inheritance of particular
alleles of the apolipoprotein E gene affects the risk of Alzheimer's disease (AD). There is evidence of increased lipid peroxidation
in CSF lipoproteins from patients with AD, but the biological significance of this observation is not known. A characteristic
of the AD brain is a disturbance of the neuronal microtubule organization. We have shown previously that 4-hydroxy-2(E)-nonenal, a major product of lipid peroxidation, causes disruption of neuronal microtubules and therefore tested whether
oxidized CSF lipoproteins had the same effect. We exposed Neuro 2A cells to human CSF lipoproteins and analyzed the microtubule
organization by immunofluorescence. In vitro oxidized human CSF lipoproteins caused disruption of the microtubule network, while their native (nonoxidized) counterparts
did not. Microtubule disruption was observed after short exposures (1 h) and lipoprotein concentrations were present in CSF
(20 μg/mL), conditions that did not result in loss of cell viability. Importantly, adult bovine CSF lipoproteins, oxidized
under identical conditions, had no effect on the microtubule organization of Neuro 2A cells. Comparison of human and bovine
CSF lipoproteins revealed similar oxidation-induced modifications of apolipoproteins E and A-I as analyzed by sodium dodecyl
sulfate-polyacrylamide gel electrophoresis and Western blotting. Fatty acid analysis revealed substantially lower amounts
of unsaturated fatty acids in bovine CSF lipoproteins, when compared to their human counterparts. Our data therefore indicate
that oxidized human CSF lipoproteins are detrimental to neuronal microtubules. This effect is species-specific, since equally
oxidized bovine CSF lipoproteins left the neuronal microtubule organization unchanged. 相似文献
15.
Piao MJ Yoon WJ Kang HK Yoo ES Koh YS Kim DS Lee NH Hyun JW 《International journal of molecular sciences》2011,12(11):8146-8160
The aim of this study was to investigate the cytoprotective properties of the ethyl acetate fraction of Sargassum muticum (SME) against ultraviolet B (UVB)-induced cell damage in human keratinocytes (HaCaT cells). SME exhibited scavenging activity toward the 1,1-diphenyl-2-picrylhydrazyl radicals and hydrogen peroxide (H(2)O(2)) and UVB-induced intracellular reactive oxygen species (ROS). SME also scavenged the hydroxyl radicals generated by the Fenton reaction (FeSO(4) + H(2)O(2)), which was detected using electron spin resonance spectrometry. In addition, SME decreased the level of lipid peroxidation that was increased by UVB radiation, and restored the level of protein expression and the activities of antioxidant enzymes that were decreased by UVB radiation. Furthermore, SME reduced UVB-induced apoptosis as shown by decreased DNA fragmentation and numbers of apoptotic bodies. These results suggest that SME protects human keratinocytes against UVB-induced oxidative stress by enhancing antioxidant activity in cells, thereby inhibiting apoptosis. 相似文献
16.
The mechanisms by which the antioxidant butylated hydroxyanisole (BHA) inhibits recombinant tumor necrosis factor alpha (rTNF-α)-induced
cytotoxicity have been studied in WEHI 164 clone 13 (WEHI) and L929 fibrosarcoma cells. When BHA was added simultaneously
with rTNF-α, it completely inhibited rTNF-α cytotoxicity in the WEHI and L929 cells. BHA also inhibited the toxicity when
added 2 h after rTNF-α in WEHI cells, suggesting that BHA inhibits some late intracellular event(s) in rTNF-α cytotoxicity.
Pretreating WEHI cells with BHA for 4 h did not decrease the binding of rTNF-α to its receptors as measured using flow cytometry.
BHA inhibited rTNF-α toxicity in the presence of actinomycin D and cycloheximide, indicating that neither mRNA nor protein
synthesis is necessary for the BHA effect. The antioxidant butylated hydroxytoluene (BHT) and indomethacin did not inhibit
the rTNF-α-induced cytotoxicity nor the rTNF-α-induced release of [3H]arachidonic acid. By comparison, BHA completely inhibited the rTNF-α-induced release of arachidonic acid, suggesting that
BHA somehow inhibits rTNF-α-induced activation of phospholipase(s). In WEHI cells, rTNF-α increased the level of protein-associated
thiobarbituric acid reactive substances (TBARS) dose-dependently. BHA, but not BHT, blocked rTNF-α-induced cytotoxicity and
rTNF-α-induced accumulation of protein-associated TBARS, suggesting that rTNF-α cytotoxicity is correlated with protein-associated
TBARS. In conclusion, the results suggest that BHA blocks some post receptor event in rTNF-α-induced cytotoxicity, and that
activation of phospholipase(s) coupled with the enzymatic formation of specific oxidized lipids could be a pivotal event in
rTNF-α-induced cytotoxicity. 相似文献
17.
José Ignacio Recio-Rodríguez Manuel A Gómez-Marcos María C Patino-Alonso Cristina Agudo-Conde Emiliano Rodríguez-Sánchez Luis García-Ortiz 《Nutrition journal》2012,11(1):1-5
Background
DNA is constantly exposed to reactive oxygen species (ROS), spontaneously arising during the normal oxygen metabolism. ROS may result in temporary as well as permanent modifications in various cellular components such as lipids, proteins and DNA, which may have deleterious consequences. Demonstrating that a dietary supplementation of antioxidants can reduce oxidative DNA damage may provide evidence for the value of such supplementation in prevention of cancer and age related diseases.Findings
The present study was conducted to address whether tomato juice protects against ROS induced by extensive physical exercise in untrained individuals. As a marker of oxidative stress, serum levels of 8-oxodG were monitored using a modified ELISA. An intervention was performed involving 15 untrained healthy subjects who performed a 20?min physical exercise at 80% of maximum pulse using an ergometer bicycle. Blood samples were taken before and one hour after the exercise. The procedure was repeated after 5?weeks with a daily intake of 150?ml tomato juice and followed by a 5?weeks wash-out period and another 5?weeks with a daily intake of tomato juice. The results indicated that a daily intake of tomato juice, equal to 15?mg lycopene per day, for 5?weeks significantly reduced the serum levels of 8-oxodG after an extensive physical exercise.Conclusion
These data strongly suggest that tomato juice has a potential antioxidant effect and may reduce the elevated level of ROS induced by oxidative stress. 相似文献18.
《Applied catalysis. B, Environmental》2005,55(1):23-30
Photocatalytic degradation of the natural oestrogens 17β-oestradiol and oestriol and the synthetic oestrogen 17α-ethynyloestradiol in water were investigated. The reactions were carried out in a quartz coil reactor coated internally with titanium dioxide (Degussa P-25). Degradation by UV light alone was also investigated. Reactions were monitored using fluorescence spectroscopy. The effect of initial concentration and the effect of light intensity on the photocatalysis and photolysis of 17β-oestradiol in water were also investigated. The results showed that photocatalysis and photolysis are capable of degrading all three oestrogens in water. Photocatalysis is much more effective than UV light alone and all reactions follow pseudo first order kinetics. The rate was found to be proportional to the square root of light intensity for photocatalysis of 17β-oestradiol. The relationship between light intensity and the rate of degradation by photolysis is linear up to a point when it starts to level off. 相似文献
19.
Raneva V Shimasaki H Furukawa Y Ueta N Yanishlieva N Aaseng JE Partali V Sliwka HR Yoshida Y Niki E 《Lipids》2002,37(7):633-640
The antioxidant action on lipid peroxidation of the synthesized selenium compounds 1-(11-selenadodecyl)-glycerol (SeG) and
1-(11-selenadodecyl)-3-Trolox-glycerol (SeIrG, where Trolox=6-hydroxyl-2,5,7,8-tetramethylchroman-2-carboxylic acid) was investigated.
We compared the reactivity of the selenium compounds toward peroxyl radicals and their inhibitory effect on lipid peroxidation,
induced by several kinds of initiating species such as azo compounds, metal ions, and superoxide/nitric oxide in solution,
micelles, membranes, and rat plasma. SeTrG, but not SeG, scavenged peroxyl radicals. SeG reduced methyl linoleate hydroperoxides
in organic solution and in methyl linoleate micelles oxidized by ferrous ion (Fe2+)/ascorbic acid. In rat plasma SeG and SeTrG decreased the formation of lipid hydroperoxides generated by hydrophilic azo
compounds. SeG and SeTrG spared α-tocopherol (α-TOH) consumption in multilamellar vesicle membranes oxidized by hydrophilic
or lipophilic initiators, and only SeTrG spared α-TOH in superoxide/nitric oxide oxidized membranes. In rat plasma oxidized
by radical initiators (either hydrophilic or lipophilic) or superoxide/nitric oxide, SeTrG suppressed α-TOH consumption, but
SeG had no effect. The two selenium-containing compounds showed inhibitory effects on lipid peroxidation that depended on
their structure, the medium where they acted, and the oxidant used. 相似文献
20.