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کاربرد نوع شرط:
- جایگاه : پژوهشی
- مجله: Iranian Journal of Pharmaceutical Sciences
- نوع مقاله: Journal Article
- کلمات کلیدی: Wastewater,ROS,Stress oxidative,Isolation Mitochondria,Scallop,Ag/ TiO2-NPs
- چکیده:
- چکیده انگلیسی: Industrial wastewater is of global concern due to its severe effects on the environment. Compared with municipal wastewater, industrial wastewater generally contains the high concentration of toxic or no biodegradable pollutants. In recently year, scientific showed that scallop could filtration wastewater. Therefore, it was decided to determine the mechanistic toxicity of wastewater contained NPs (Ag and TiO2) towards isolated mitochondria via reliable methods. Isolated muscle scallop mitochondria were obtained by differential ultracentrifugation on before and after exposure to wastewater. Our results showed that two NPs (Ag and TiO2) induced mitochondrial dysfunction via an increase in mitochondrial reactive oxygen species (ROS) generation, lipid peroxidation (LPO) and mitochondrial membrane potential (MMP) collapse. Finally, Ag-NPs and TiO2-NPs have reduced the level of glutathione (GSH) and also induced apoptosis. Our results suggest that wastewater contained NPs -induced toxicity is the result of a disruptive effect on the mitochondrial respiratory chain, increasing the chance of cell death signaling.
- انتشار مقاله: 28-01-1398
- نویسندگان: Farahnaz Tanbakosazan,Pirouz Derakhshi,Parviz Abroomand Azar,Khadijeh Ashtari,Parvaneh Naserzadeh,Enayatollah Seydi,Jalal Pourahmad
- مشاهده
- جایگاه : پژوهشی
- مجله: Iranian Journal of Pharmaceutical Sciences
- نوع مقاله: Journal Article
- کلمات کلیدی: Apoptosis,Hepatocellular carcinoma,Hepatocytes,Enhydrina schistosa,Mitochondria, Reactive Oxygen Species
- چکیده:
- چکیده انگلیسی: Common techniques for the treatment of Hepatocellular carcinoma (HCC) have not been successful, and thus the design and discovery of new compounds with better anti-cancer function are needed. Snake venom is among the most important compounds used by researchers to the treatment of various cancers. This study was designed to evaluate the toxicity effect of Persian Gulf snake venom (Enhydrina schistosa) on hepatocytes and mitochondria isolated from HCC rats model. HCC has been induced in rats with diethylnitrosamine (DEN) and 2-acetylaminofluorene (2-AAF). Then rat hepatocytes were isolated with collagen perfusion technique. The results showed that E. schistosa (5, 10, 20 and 40 µg/ml) increases the level of reactive oxygen species (ROS) generation, collapse in mitochondrial membrane potential (MMP), swelling in mitochondria, and cytochrome c release only in hepatocytes and mitochondria isolated from the HCC group. These results proposed that E. schistosa could be considered as a promising complementary therapeutic agent for the treatment of HCC.
- انتشار مقاله: 26-03-1398
- نویسندگان: Enayatollah Seydi,Pardis Tajarri,Parvaneh Naserzadeh,Jalal Pourahmad Jaktaji
- مشاهده
- جایگاه : پژوهشی
- مجله: Iranian Journal of Pharmaceutical Sciences
- نوع مقاله: Journal Article
- کلمات کلیدی: Mitochondria,MTBE,morphology,embryotoxicity,Placenta,Mouse fetus
- چکیده:
- چکیده انگلیسی: Although the biokinetics, metabolism, and chemical toxicity of methyl tert-butyl ether are well known, little attention was paid to the potential toxic effects of MTBE on reproduction and development in mammals. To evaluate the effects of MTBE on pregnant animals, two groups (control and test) of NMRI mice were chosen. In test group 500 and 1000 mg/Kg of it were administered intraperitonealy at 11 days of gestation and in control group no injection was made. Caesarean section was performed at 15 days of the gestation, and the fetus and placentas were examined externally. Based on our morphological results, MTBE caused significant increase (p < 0.05) in the weight of fetuses and the weight of placentas, the diameter of placentas and crown-rump length of fetuses. Also, our mitochondrial results showed significant (p < 0.05) increase in mitochondrial swelling, ROS formation and also significant (p < 0.05) decreased in MMP on mitochondria isolated from liver and brain in test group. These results suggest that MTBE through ROS formation may induce the mitochondrial dysfunction which in turn leads to inhibition of angiogenesis and morphological alterations in fetus of mouse.
- انتشار مقاله: 29-03-1397
- نویسندگان: Mehrdad Faizi,Fatemeh Jamal,Baharak Mohammadzadeh Asl,Parvaneh Naserzadeh,Zeinab Saadabadi,Ahmad Salimi,Jalal Pourahmad Jaktaji
- مشاهده
- جایگاه : پژوهشی
- مجله: Iranian Journal of Pharmaceutical Sciences
- نوع مقاله: Journal Article
- کلمات کلیدی: Mitochondria,Apoptosis,Brain,Atorvastatin,CoQ10,E vitamin
- چکیده:
- چکیده انگلیسی: Background: Although the bio kinetics, metabolism and chemical toxicity of Atorvastatin are well known, until recently little attention was paid to the potential neurotoxic effect of Atorvastatin (Atv). Regarding the concrete evidences indicating Atv may reduce Coenzyme Q10 (CoQ10) levels through blockage of metalonate cycle, the present work aims to determine if Atorvastatin may provide toxic effects on brain mitochondria and whether its supplementation with two lipidicantioxidants, CoQ10 and Vit E may improve such outcomes.
Methods: to evaluate mitochondrial toxicity, male NMRI mice were first treated with Atorvastatin(bo; 20 and 60 mg/kg) every other day with or without supplementation with CoQ10 (200 mg/kg) or Vit E (40 u/kg). After a period of 4 weeks, the animals were euthanized and brain cortices were harvested ad subjected to mitochondria isolation procedure. ROS release, mitochondrial membrane potential (MMP) and cytochrome c release were performed to precisely address the probable mitochondrial injury.
Findings: Our data showed increased ROS formation, MMP collapse, mitochondrial swelling and cytochrome c release in Atorvastatin treated mice, suggesting that mitochondrial ROS formation and apoptosis signaling are likely involved in Atorvastatin neurotoxicity. Importantly according to the data from animals receiving either CoQ10 or Vit E, supplementation with these lipophilic antioxidants, remarkable reverted the corresponding Atorvastatin mitochondrial toxicity markers.
Concusion: Conclusively the present work addresses chronic Atorvastatin toxic effects on brain mitochondria and supports advantages of Vit E or CoQ10 supplementation. Whether such neurotoxic effect is correlated with CoQ10 depletion or if the improving effects of the due supplementation contribute toAtorvastatin receiving patients, needs more investigations.- انتشار مقاله: 05-09-1395
- نویسندگان: Sanaz Nasoohi,Parvaneh Naserzadeh,Nafiseh Rahmanabadi,Banafsheh Saiid,Jalal Pourahmad Jaktaji
- مشاهده
- جایگاه : پژوهشی
- مجله: Iranian Journal of Pharmaceutical Sciences
- نوع مقاله: Journal Article
- کلمات کلیدی: Mitochondria,reactive oxygen species,hepatotoxicity,Mercaptopurine,lysosome,ACMS
- چکیده:
- چکیده انگلیسی: 6- Mercaptopurine (6-MP) is widely used in clinic as an immunosuppressive for treatment of acute lymphocytic leukemia, Crohn's disease, and ulcerative colitis with documented unpredictable hepatotoxicity. The potential molecular cytotoxic mechanisms of 6-MP against isolated rat hepatocytes were searched in this study using “Accelerated Cytotoxicity Mechanism Screening (ACMS)” techniques. The concentration of 6-MP required to cause 50% cytotoxicity in 2 hour at 37∘C was detected to be 400 µM. A significant increase in 6-MP induced cytotoxicity and reactive oxygen species (ROS) formation, % mitochondrial membrane potential (MMP), lysosomal damage was observed. The addition of chloroquine (lysosomotropic agent), L-carnitine (inhibitor of membrane permeability transition (MPT), Diphenyleneiodonium (DPI) as an inhibitor of production of superoxide and H2O2 by mitochondria and Dimethyl sulfoxide (DMSO) as a radical scavenger decreased 6-MP-induced cytotoxicity, ROS formation, collapse of MMP, lysosomal damage. Results from this study suggest that 6-MP -induced cytotoxicity in isolated rat hepatocytes due to ROS formation, mitochondrial and lysosomal damages that resulted in crosstalk toxicity between mitochondrial and lysosomal damage and finally cell death.
- انتشار مقاله: 13-02-1395
- نویسندگان: Ahmad Salimi,Melina Ramandoost,Jalal Pourahmad Jaktaji
- مشاهده
- جایگاه : پژوهشی
- مجله: Iranian Journal of Pharmaceutical Sciences
- نوع مقاله: Journal Article
- کلمات کلیدی: Mouse fetus,Developmental toxicity,PFOS,Neurobehavioral toxicity,Isolated mitochondria,Brain anomaly
- چکیده:
- چکیده انگلیسی: Perfluorooctanesulfonate (PFOS) is a widely spread environmental contaminant. It accumulates in the brain and has potential neurotoxin effects. Due to chemical properties, PFOS shows persistency in the environment and therefore has potential hazardous effect. The risk of possible intra uterine exposure to PFOS poses a health concern for developmental effects. The goal of this study was survey of histological and behavioral changes made by PFOS in pregnant mice and their fetuses using common behavioral assays and H&E staining. In the present study doses of PFOS (1,10,20 mg/kg) given orally to pregnant mouse from gestational day (GD) 0 to GD14; then on the day 15, Behavioral experiments including (open field and passive avoidance) were used to assess toxic behavioral changes such as memory impairment and anxiety. After behavioral evaluations fetuses were dissected on day 15 of gestation and morphological and histological studies on pregnant mouse brain and her fetus were carried out using haematoxylin-eosin staining method. Our findings showed that PFOS can induce neurotoxicity in pregnant mouse especially by induction of abnormalities in dentate gyrus of hippocamps and disruption of neurobehavioral functions .Besides in her fetus; PFOS produced significant changes in brain, liver and thyroid gland in comparison with untreated control mouse fetus. As a conclusion, PFOS can cause both neurobehavioral and developmental toxicity in pregnant mouse and her fetus.
- انتشار مقاله: 10-09-1394
- نویسندگان: Freshteh Mehri,Mehrdad Faizi,Farzad Kahrizi,Baharak Mohammadzadeh Asl,Jalal Pourahmad Jaktaji
- مشاهده
- جایگاه : پژوهشی
- مجله: Iranian Journal of Pharmaceutical Sciences
- نوع مقاله: Journal Article
- کلمات کلیدی: Cigarette smoking extracts (CSE), Cytochrome c release, isolated mitochondria,mitochondrial dysfunction
- چکیده:
- چکیده انگلیسی: Cigarette smoking is one of the main risk factors for premature human death associated to a variety of respiratory and vascular diseases, and cancer due to containing Hundreds of toxicants. Rat mitochondria were obtained by differential ultracentrifugation and incubated with different concentrations (1, 10 and 100%) of standardized cigarette smoke extract (CSE). Our results showed that cigarette smoke extract (CSE) induced a rise in mitochondrial ROS formation and mitochondrial membrane potential decrease before mitochondrial swelling ensued in isolated eye and kidney mitochondria. Disturbance in oxidative phosphorylation was also confirmed by decrease in ATP concentration in the CSE treated mitochondria. In addition, collapse of mitochondrial membrane potential (MMP) and mitochondrial swelling caused release of cytochrome c via outer membrane rupture or MPTpore opening. Our results suggested that cigarette smoke induced toxicity in both external directly exposed and visceral tissues is the result of disruptive effect on mitochondrial respiratory chain that leads to ROS formation, lipid peroxidation, mitochondrial membrane potential decline and cytochrome c expulsion which starts apoptosis signaling and cell loss.
- انتشار مقاله: 24-04-1393
- نویسندگان: Parvaneh Naserzadeh,Jalal Pourahmad
- مشاهده
- جایگاه : پژوهشی
- مجله: Iranian Journal of Pharmaceutical Sciences
- نوع مقاله: Journal Article
- کلمات کلیدی: Apoptosis,cytochrome C,Atorvastatin calcium,fetal mitochondria,morphological anomalies,Embryotoxicity Introduction
- چکیده:
- چکیده انگلیسی: Although the biokinetics, metabolism, and chemical toxicity of atorvastatin calcium are well known, until recently little attention was paid to the potential toxic effects of atorvastatin calcium on re-production and development in mammals. In recent years, it has been shown that atorvastatin calcium is a developmental toxicant when given orally or subcutaneously (SC) to mice. Decreased fertility, embryo/fetal toxicity including teratogenicity, and reduced growth of the offspring have been observed following atorvastatin calcium exposure at different gestation periods. On the other hand, an in vitro study using fetal isolated mitochondria nowadays has been recognized as a confident tool to evaluate the developmental toxicity of a number of chemicals. Although the developmental toxicity induced by atorvastatin has been investigated, the precise cellular mechanism of atorvastatin -induced embryo-toxicity has not been thoroughly recognized yet. For investigating the effects of atorvastatin calcium on pregnant animals, three groups (control, sham and test) of NMRI mice were chosen. In test group (50mg/kg,100mg/kg and 150mg/kg)of atorvastatin calcium were administered intraperitonealy at 11 day of gestation, in sham group only normal saline injected to interior peritoneum as indicated in the test group and in Control group which was considered as the comparison base line of our research, no injection was made. Caesarean sections were performed at 15 day of the gestation; and their placentas were examined externally. Based on our results atorvastatin calcium caused significant external anomalies, and caused a significant decrease (p<0.001) in the weight and diameter of placentas, the number of the embryos, their body weight and crown-rump length of fetuses.
- انتشار مقاله: 11-08-1392
- نویسندگان: Farhad Emami,Baharak Mohammadzadeh Asl,Enayatollah Seydi,Mohammad Zargar,Parvaneh Naserzadeh,Jalal Pourahmad Jaktaji
- مشاهده
- جایگاه : پژوهشی
- مجله: Iranian Journal of Pharmaceutical Research
- نوع مقاله: Journal Article
- کلمات کلیدی: Mitochondria,Antioxidant,Nephrotoxicity,Protection,Depleted uranium,Beta-glucan
- چکیده:
- چکیده انگلیسی: Considerable evidence suggests that mitochondrial dysfunction contributes to the toxicity of uranyl acetate (UA), a soluble salt of depleted uranium (DU). We examined the ability of the two antioxidants, beta-glucan and butylated hydroxyl toluene (BHT), to prevent UA-induced mitochondrial dysfunction using rat-isolated kidney mitochondria. Beta-glucan (150 nM) and BHT (20 nM) attenuated UA-induced mitochondrial reactive oxygen species (ROS) formation, lipid peroxidation and glutathione oxidation. Beta-glucan and BHT also prevented the loss of mitochondrial membrane potential (MMP) and mitochondrial swelling following the UA treatment in isolated mitochondria. Our results show that beta-glucan and BHT prevented UA-induced mitochondrial outer membrane damage as well as release of cytochrome c from mitochondria. UA also decreased the ATP production in isolated mitochondria significantly inhibited with beta-glucan and BHT pre-treatment. Our results showed that beta-glucan may be mitochondria-targeted antioxidant and suggested this compound as a possible drug candidate for prophylaxis and treatment against DU-induced nephrotoxicity.
- انتشار مقاله: 19-06-1391
- نویسندگان: Fatemeh Shaki,Jalal Pourahmad
- مشاهده
- جایگاه : پژوهشی
- مجله: Asian Pacific Journal of Cancer Prevention
- نوع مقاله: Journal Article
- کلمات کلیدی: Mitochondria,Apoptosis,Melanoma,Turbo coronatus,Gel filtration
- چکیده:
- چکیده انگلیسی: Objective: A variety of approaches such as surgery, chemotherapy, radiotherapy, hormonal therapy and
immunotherapy are used to treat melanomas, but unfortunately in most case, the response is very weak and often side
effects are serious. This study concerns selective toxicity of an extract of Turbo coronatus on cells and mitochondria from
a syngeneic mouse model of melanoma. Methods: Cells and mitochondria isolated from extra tumoral and melanoma
tissues were exposed toa T. coronatus crude extract and fractions obtained by gel-filtration chromatography and assayed
for mitochondrial and cellular parameters. Result: Crude extract (375, 750 and 1,500 μg/ml) and fraction 1; F1; (275,
550 and 1100 μg/ml) of T. coronatus extract induced a significant (p<0.05) increase of the reactive oxygen species
(ROS) level, swelling of mitochondria, collapse of mitochondrial membrane potential (MMP), release of cytochrome
c and caspase-3 activation only in the mitochondria and cells obtained from melanoma but not extra tumoral tissues. In
addition, the F1 fraction decreased the percentage of viable cells and induced apoptosis in melanoma cells. Conclusion:
For the first time we could demonstrate that the F1 fraction of a T. coronatus extract, selectively induces ROS mediated
cytotoxicity by directly targeting mitochondria in melanoma tissues and it may be a suitable candidate for novel drug
treatment of malignant melanomas.- انتشار مقاله: 16-12-1396
- نویسندگان: Fatemeh Zangeneh,Amir Vazirizadeh,Mohammad Reza Mirshamsi,Amir Fakhri,Mehrdad Faizi,Jalal Pourahmad
- مشاهده