جستجوی مقالات مرتبط با کلیدواژه « Reactive Oxygen Species (ROS) » در نشریات گروه « پزشکی »

Until recently, a conventional chemotherapy regimen for Acute lymphoblastic leukemia (ALL) is considered an efficient therapeutic method in children. However, suboptimal long-term survival rates in adults, disease relapse, and drug-induced toxicities require novel therapeutic agents for ALL treatments. Today, natural products with pharmacological benefits play a significant role in treating different cancers. Among the most valued natural products, honey bees’ royal jelly (RJ) is one of the most appreciated which has revealed anti-tumor activity against different human cancers. This study aimed to evaluate anti-leukemic properties and the molecular mechanisms of RJ cytotoxicity on ALL-derived Nalm-6 cells.

The metabolic activity was measured by MTT assay. Apoptosis, cell distribution in the cell cycle, and intracellular reactive oxygen species (ROS) level were investigated using flow cytometry analysis. Moreover, quantitative real-time PCR (qRT-PCR) was performed to scrutinize the expression of various regulatory genes. 

RJ significantly decreased the viability of Nalm-6 cells but had no cytotoxic effect on normal cells. In addition, RJ induced ROS-mediated apoptosis by up-regulating pro-apoptotic genes while decreasing anti-apoptotic gene expression. The results outlined that ROS-dependent up-regulation of FOXO4 and Sirt1 inhibits the cells’ transition to the S phase of the cell cycle through p21 up-regulation. The qRT-PCR analysis of autophagy-related gene expression also demonstrated that RJ induced BECN1 mediated autophagy in Naml-6 cells.

Taken together, this study showed that RJ can be utilized as a potent natural substance to induce ALL cells’ programmed cell death. However, further studies are required to examine this compound’s pharmaceutical application.

Low-temperature plasma (LTP) has demonstrated great potential in biomedicine, especially in cancer therapy in-vivo and in-vitro. Plasma activated water (PAW) as an indirect plasma therapy is a significant source of reactive oxygen and nitrogen species (RONS) which play an important role in apoptosis induction in cancer cells. In this study, Helium (He) plasma jet operating in 0.75 W and 20 kHz as dissipated power and frequency, respectively, is used as the cold plasma source. The electrical, thermal, and spectroscopic properties of (He) plasma jet and pH as well as the conductivity and temperature of PAW samples, are investigated. The concentration of hydrogen peroxide (H2O2), nitrite (NO2 -) and nitrate (NO- 3), which are produced in water as long-lived anticancer RONS, was measured 471.6, 7.9 and 93.5 μM, respectively after 6 min of plasma treatment. Alamar Blue and flow cytometry assays were employed to investigate the B16F10 cancer metabolic activity and apoptosis. These data support that cold atmospheric plasma (CAP) can produce a certain concentration of anti-cancer agents in water and induce apoptosis in melanoma cancer cells due to RONSs via activating the caspase 3 pathway.

Antioxidants are substances that are available in various natural food products, which play a vital role in reducing body cell damage caused by free radical formation. An imbalance between antioxidants and free radicals contributes to an oxidative stress in the human body. The electron acceptability of O2 produced Reactive Oxygen Species (ROS). The imbalance equilibrium between the production of reactive oxygen species (ROS) and the purification supports a rise in the ROS levels, which is the key cause of disrupted cellular activity. A recent review of excessively mild antioxidants, processes of movement, and their role in many human illnesses.

Caused by an imbalance in the body’s oxidant and antioxidant status, oxidative stress can give rise to tissue damage and exacerbation of many diseases.

This study investigated the oxidative stress markers in patients with fractures and healthy subjects.

In a cross-sectional case-control study, 40 patients with fractures admitted to an orthopedic ward and 40 healthy, nonfractured patients were selected using convenience sampling. Serum was analyzed for oxidant and antioxidant activities based on standard methods. P < 0.05 was considered statistically significant.

There was a significant difference in mean TAC between the case (748.2 ± 302.83 µmol/L) and control (984.90 ± 207.02 µmol/L) groups (P = 0.003). The mean MDA was 16.61 ± 4.16 µmol/L in the case group and 18.45 ± 5.43 µmol/L in the control group (P = 0.09). The mean SOD was 63.41 ± 16.67 U/g Hb in the case group and 58.54 ± 21.83 U/g Hb in the control group (P = 0.2). There was no significant difference between the two groups in terms of BMI and other variables.

A significant difference existed in TAC between the two groups, which indicated increased oxidative stress in patients. However, oxidative stress could occur before and after undergoing fractures. The results suggested a slight, but not significant, difference between the two groups in the SOD and MDA scores. More conclusive results are required to determine the enzymatic and non-enzymatic markers of oxidative stress in larger sample sizes and during different stages of treatment.

It is unquestionable that the employment of nano technology in every enterprise depicts a future for sustainable development due to the cheap and clean availability of nano materials. Evidently the researchers have largely centered on the blessings of the nano materials in cosmetics and food industries failing to center the negative effects it can impose on human fitness and environment. Titanium dioxide (TiO2) is one such nano particle that despite its elite properties is responsible for generation of oxidative stress. This review compiles some significant research carried out for the assessment of accelerated oxidative stress markers and the presence of Titania traces in human samples and sea organisms manifesting how they are damaging the living mechanisms. The elimination of the nanoparticles into the environment somehow advances towards land and water contaminating the soil, rivers and oceans having a derogatory effect on the natural running phenomena of soil organisms, sea algae and mussels. This review presents the latest findings and indicates making some strategies for reducing the use of the nano materials to a significant but limited amount making sure that it is not liable to any impairment to the humans and the surroundings.

Pentagamavunon-1 (PGV-1) is a curcumin analogue that shows cytotoxic activity invarious cancer cells. In this study, we evaluated the effect of PGV-1 on a highly metastatic breastcancer cell line, the 4T1 cells, as an anti-metastatic and anti-proliferative agent. Cell viability was evaluated using MTT assay; while cell cycle profile, apoptosisincidence, and ROS intracellular level were determined by flow cytometry. Cell senescence wasobserved under senescence-associated-β-galactosidase (SA-β-gal) staining assay. The expressionof matrixmetalloproteinase-9 (MMP-9) was determined using immunoreaction based-ELISA,while other proteins expression were detected using immunoblotting. Curcumin and PGV-1 showed cytotoxic effects on 4T1 cells with IC50 value of 50 and4 μM, respectively. The cytotoxic activity of PGV-1 was correlated to the induction of G2/M cellcycle arrest and cell senescence. Furthermore, PGV-1 increased the accumulation of intracellularROS level. We also revealed that PGV-1 bound to several ROS-metabolizing enzymes,including glyoxalase I (GLO1), peroxiredoxin 1 (PRDX1), N-ribosyldihydronicotinamide:quinone reductase 2 (NQO2), aldo-keto reductase family 1 member c1 (AKR1C1). As an antimetastaticagent, PGV-1 showed less inhibitory effect on cell migration compared to curcumin.However, PGV-1 significantly decreased MMP-9 protein expression in a dose-dependentmanner suggesting it still potent to inhibit metastatic cells. Overall, our findings suggest that PGV-1 is potential to be developed as an antiproliferativeand anti-metastatic agent.

Genistein, a soy isoflavone, exhibits a biphasic effect on cells proliferation withsome different effects between ER-alpha and ER-beta. The objective of this present study is todetermine the modulatory effect based on cell cycle progression under genistein treatment incombination with 17-β estradiol (E2) on CHO-K1 cells. The effect of genistein 0.1-100 μM on cells proliferation was examined by MTT assay.The modulation of genistein and estradiol (E2) on cell cycle and apoptosis were observed byusing flowcytometry with PI and PI/AnnexinV staining, respectively. Moreover, the effect ofgenistein and E2 on senescence cells, and ROS level were determined by senescence-associatedβ-galactosidase (SA β-gal) staining and by using flowcytometry with 2’, 7’–dichlorofluorescindiacetate (DCFDA) staining, respectively. The expression level of the cell cycle and senescenceprotein markers were observed by immunoblotting. Single treatment of genistein at physiologically achievable (low) concentration (<2 μM)induced proliferation of CHO-K1 cells while at a pharmacological (high) concentration (50 and100 μM) suppressed cells proliferation. Interestingly, treatment of genistein at the physiologicalconcentration in combination with E2 for 24, 48 and 72 h decreased cells viability on CHO-K1cells compared to untreated cells. Further analysis of the cells showed that 50 μM genisteininduced G2/M phase accumulation and induced apoptosis. Moreover, genistein induced cellsenescence and increased ROS level. Immunoblotting analysis showed the decreasing of ERalpha,Bcl2, and ppRb protein level upon treatment of 1 μM Gen and 1 nM E2. Our results suggest that the cell proliferation inhibitory mechanism of genistein atpharmacological concentration involved the induction of cell senescence, and the elevationof ROS level. Moreover, the decreased of cells proliferation upon treatment of physiologicalconcentration of genistein in combination with E2 may be correlated with the alteration of ERexpression.

Lead is a heavy metal used in industries in developing countries. Lead exposure remains a widespread problem. Lead may induce molecular damage in the kidney as a consequence of Reactive Oxygen Species (ROS) formation, induction of caspase-3, and apoptosis. Thirty male Wistar rats (Mean±SD weight: 300±20 g) were randomly divided into 3 equal groups: control (normal saline, oral), lead group (lead 100 mg/kg/d, oral) and lead+L-Carnitine (lead 100 mg/kg+L-Carnitine 200 mg/kg, intraperitoneal injection) for one week. At the end of the experiment, plasma creatine kinase activity, plasma creatinine and urea concentrations and plasma Superoxide Dismutase (SOD), Glutathione Peroxidase (GPx), catalase and nitric oxide levels were determined. Glutathione and malondialdehyde levels in renal tissue were also measured. Creatine kinase, creatinine and urea levels increased significantly, in the group treated with lead (P<0.05), compared to the control group. Administration of L-Carnitine in (Lead+carnitine treated group) significantly (P<0.05) decreased creatine kinase activity and plasma urea and creatinine contents. Enzymatic activity (SOD, GPx, and CAT) decreased significantly in the lead group, in comparison with the control group (P<0.05). Treatment with L-Carnitine significantly retrieved the depletion in enzyme activity (P<0.05). However, there were no significant differences in the GPx parameter between the Lead+carnitine group, in comparison with the control group. L-Carnitine administration in rats with lead-induced nephropathy led to improved kidney protection, due to the reduction of Lipid Peroxidation (LPO). Furthermore, L-Carnitine prevents the adverse effects of Reactive Oxygen Species (ROS), which is an important biomolecules mechanism

Perfluorinated compounds (PFCs) such as perfluorooctanesulfonate (PFOS) are stable chemicals that accumulate in biological matrix. Toxicity of these compounds including immunotoxicity has been demonstrated in experimental models and wildlife. Although limited number of studies examined the effects of PFOS on human lymphocytes but so far no research has investigated the complete mechanisms of PFOS cytotoxicity toward human lymphocytes. The main goal of this investigation was to find out the mechanisms underlying the cytotoxic effect of PFOS toward human lymphocytes using accelerated cytotoxicity mechanisms screening (ACMS) technique. Human lymphocytes were isolated from blood of healthy donors using Ficoll-paquePLUS standard method. Cell viability was determined following 12 h of incubation of human lymphocytes with 100-500 μM PFOS. Our results showed that IC50 concentration (163.5 μM) of PFOS reduced viability of human lymphocytes approximately 50% via increased ROS formation, lipid peroxidation, glutathione depletion and damage to cell sub organelles such as mitochondria and lysosomes. Besides, in this study we demonstrated involvement of cellular proteolysis and activation of caspase-3 in PFOS induced lymphocyte cytotoxicity. We finally concluded that at environmentally related concentration, PFOS can induce toxic effect toward human lymphocytes through induction of oxidative stress and damage to cell sub organelles.

Diabetes mellitus (DM) is characterized by the presence of hyperglycemia. It has been documented that oxidative stress and reactive oxygen species (ROS) production have a key role in the pathogenesis of diabetes and its complications. Neutrophils as a part of immune system produce ROS, neutrophils function might be altered in diabetes. Lamium album is known to have antioxidant, and free radical scavenging actions. The aim of the present study was to evaluate the potential effect of L. album on mitochondrial ROS production from circulating neutrophils in diabetic rats.
Twenty-one male Wistar rats were randomly divided into three groups: normal control rats receiving daily saline; diabetic control rats receiving daily saline; and diabetic rats treated daily with hydroalcoholic extract of L. album (100 mg/kg) for 28 days. On the 28thday of treatment, whole blood samples were obtained and mitochondrial ROS of neutrophils were measured by dihydrorhodamine (DHR) flow cytometric method. Also, fasting blood sugar (FBS) was measured.
Mitochondrial ROS didn’t show any significant differences among diabetic rats treated with L. album extract, diabetic control rats, and normal control rats (P=0.8). Serum glucose in diabetic control was significantly higher than normal control rats (P=0.0001). However, L. album caused a remarkable decrease in serum glucose of diabetic rats (P=0.03).
According to the present findings, it seems that L. album at a dose of 100 mg/kg could not decrease mitochondrial ROS production from neutrophils in diabetic rats. Further studies considering higher concentrations of L. album are appreciated to evaluate its impact on the production of mitochondrial ROS along with extracellular ROS in diabetes condition.

Induction of cellular response after exposure to electromagnetic fields is limited to coherent fields. An incoherent noise field is supposed to suppress the bioeffects of regular RF electromagnetic fields. The purpose of this study was to investigate the effect of GSM mobile phone-induced radiofrequency (RF) on the induction of oxidative stress in SP2/0 cell line. This study was also an attempt to assess whether these RF-induced effects can be blocked by superposing the RF radiation and an incoherent magnetic noise. Three groups of cultured cells were used in this study. The cells in the first group were only exposed to RF radiation emitted from a mobile phone simulator. The second group was only exposed to an incoherent noise field and the third group was simultaneously exposed to RF radiation and incoherent noise field. The exposure duration in all groups was 2 hours. The level of ROS production in the cells was quantified by the CM-H2DCFDA fluorescence probe, using flow cytometry technique. Although our results showed increased ROS production after exposure to 900 MHz RF radiation, superposition of 900 MHz RF and the incoherent noise fields did not lead to increased levels of ROS in any experiment. However, the differences between RF exposure group and superposition of RF and noise exposure group were not statistically significant. Altogether our results cannot support the neutralizing effect of noise theory but may confirm the concept that just the coherent fields can be bioeffective while the incoherent noise fields cannot cause any biological effects.

The present study was designed to investigate the protective effect of ethanol extracts from Lindera coreana leaves (LCE) on UVB-induced oxidative stress in HaCaT keratinocytes. The HaCaT cells were pretreated with LCE for 24 h and then exposed to UVB (20 mJ/cm2) for 2 h. UVB significantly decreased the cell viability (p<0.05). LCE did not exhibit significantly cytotoxic effects and increased the viability of the HaCaT cells in a concentration-dependent manner. To further investigate the protective effects of LCE on UVB-induced oxidative stress in HaCaT cells, the cellular levels of reactive oxygen species (ROS), lipid peroxidation and endogenous antioxidant enzymes, including catalase (CAT), superoxide dismutase (SOD) and glutathione peroxidase (GSH-px), were analyzed. LCE decreased the intracellular levels of ROS and lipid peroxidation and increased the activity of antioxidant enzymes. These results suggest that LCE exerted cytoprotective activity against UVB-induced oxidative stress in HaCaT cells through the inhibition of lipid peroxidation, reduction of ROS levels and stimulation of antioxidant enzymes activities. In addition, LCE also decreased the TNF-α, IL-1β and IL-6 levels in UVB-irradiated HaCaT cells.

Bronchial asthma is the common chronic inflammatory disease and is characterized by chronic airway inflammation, airway remodeling, and airway hyperreactivity (AHR). Aim of this study was to investigate the effects of mitochondrial ATP-sensitive potassium channels (MitoKATP) on the proliferation and secretion of human airway smooth muscle cells (HASMCs). HASMCs were treated with the serum from asthmatic patients to establish HASMCs asthma model of passive sensitization. Rhodamine 123 (R-123) and 2,7-dichloro-dihydrofluorescein diacetate (DCFH-DA) fluorescence staining were used to detect mitochondrial membrane potential (Δψm) and the content of reactive oxygen species (ROS) in the cells, respectively.The cell counting was used to detect cell proliferation, and RT-PCR was used to detect the expression of TGF-β1 mRNA.In the normal + Diazoxide group, the fluorescence intensity of R-123, ROS content, cell proliferation and TGF-β1 expression were enhanced, compared with the normal control group (p<0.05). There were no significant differences between the normal + 5-hydroxydecanoate (5-HD) group and the normal control group. In the asthma model control group, the fluorescence intensity of R-123, ROS content, cell proliferation and TGF-β1 expression were enhanced, compared with normal control group, (p<0.05). The aforementioned indices were enhanced in the asthma model + Diazoxide group, when compared with the asthma model control group, whereas these indices were attenuated in the asthma model + 5-HD group, when compared with the asthma model control group (p<0.05).In conclusion, asthma could activate MitoKATP channels in HASMCs, promote HASMC proliferation and TGF-β1 expression.

Arsenic exposure mainly through food and water has been shown to be associated with increased incidence of numerous cancers and non-cancer harmful health. It is also used in cancer chemotherapy and treatment of several cancer types due to its apoptogenic effects in the various cancer and normal cell lines. We have already reported that liver is the storage site and important target organ in As (III) toxicity and recently, it has been suggested that hepatic toxicity of arsenic could be resulted from impairment of the liver mitochondria. In this study, interaction of As (III) with freshly isolated rat mitochondria was investigated. We determined different mitochondrial toxicity factors as well as mitochondrial sources of ROS formation using specific substrates and inhibitors following addition of As (III) to the mitochondria. Our results showed that arsenic (III) increased mitochondrial ROS formation, lipid peroxidation and mitochondrial membrane potential collapse, cytochrome c release and mitochondrial swelling in a concentration dependent manner. Addition of As (III) in to the isolated mitochondria, inhibited complexes I and II leading to disruption of mitochondrial electron transfer chain, decreased mitochondrial ATP content and ROS formation.

Reactive oxygen species (ROS) are a group of free radicals that in excessive amounts have negative influence on sperm quality and function.

To study the effect of varicocele and its severity on the level of ROS in infertile men with clinical varicocele.

In this controlled prospective study, 42 men with clinically diagnosed left varicocele and 30 fertile men were studied. Patients were asked about history of urogenital infection, using any antioxidant medication and smoking. Grade of varicocele was determined by physical examination. Levels of ROS in seminal plasma were measured in each group by a chemiluminiscence assay. The sperm parameters were also determined and compared in different groups.

The ROS levels were significantly higher in patients with varicocele than normal men (mean: 1575.42 RLU (Radio Luminescence Unit) vs. 53.79 RLU, p=0.005). In total 20 patients had grade I, 20 patients grade II and 2 patients had grade III varicocele. The mean ROS levels were 669.12 RLU, 2406.87 RLU and 2324 RLU in patients with grade I, II and III varicocele respectively (p=0.144). In case group, 15 patients were smoker and 27 were non-smokers. The mean ROS levels in patients with the history of smoking was 1367.71 RLU while in non-smokers it was 897.672 RLU (p=0.729).

Our study showed that increased levels of ROS production in the seminal fluid can be an important factor in the etiology of male infertility in patients with varicocele, and this effect is more prominent with higher grade of varicocele.

Reactive Oxygen Species (ROS) are a group of free radicals that in excessive amounts have negative influence on sperm quality and function.

We compared ROS levels in seminal plasma of infertile men with this level in healthy donors. We also determined the ROS level in semen of infertile men according to the etiology of infertility, and also the effect of smoking on its level.

In total, 63 infertile patients and 63 healthy donors as control were selected. Complete physical examination, semen analysis, scrotal sonography and hormone assay were done for all patients. Azoospermic patients were excluded from the study. ROS level in semen was measured by chemiluminescence assay in both groups. Patients also were divided in two groups according to the etiology of infertility.

The mean age of normal subjects and infertile men were 30.78±3.73 years and 31.43±6.60 years respectively. The mean ROS level in normal men was 180.05 RLU (Relative light unit), while this was 1852.04 RLU in infertile patients, which is significantly higher in case group (p=0.000). Fifty patients had varicocele and in 13 patients no specific etiology was found. The mean ROS level in varicocele patients was 2215.42 RLU and in unknown group was 454.44 RLU (p=0.048).

Our study showed that the level of ROS in seminal fluid of infertile men is significantly higher than fertile donors and also in infertile patients with varicocele it is higher than patients with unknown cause.