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Objective: The present study examined effects of resistance training (RT) and resveratrol (RES) alone and together on acrylamide (AC)-induced memory impairment in rats. Materials and Methods: Animals were divided into 6 groups: (1) Control group which received normal saline intraperitoneally (ip) daily for 8 weeks; (2) Scopolamine (SCO) group which received SCO (1 mg/kg/day, ip) for 8 weeks; (3) AC group which received AC (5 mg/kg/day, ip) for 8 weeks; (4) AC + RT group which received AC (5 mg/kg/day, ip) for 8 weeks and performed RT (5 days a week for 8 weeks); (5) AC + RES group which received AC (5 mg/kg/day, ip) and RES (1 mg/kg/day, ip) for 8 weeks; and (6) AC + RT + RES group which received AC (5 mg/kg/day, ip) and RES (1 mg/kg/day, ip) for 8 weeks and performed RT (5 days a week for 8 weeks). On day 53, animal training began in the Morris Water Maze (MWM) and 24 hr after the last training, the probe test was performed. Results: RT and RES alone did not significantly affect escape latency or traveled distance increased by AC. However, concomitant RES and RT treatment significantly reduced these parameters compared to the AC group. Co-treatment with RES and RT also significantly increased the time spent in the target quadrant compared to the AC group. Lipid peroxidation was reduced in the AC+RES and AC+RT+RES groups compared to the AC group. Conclusion: It seems that daily co-treatment with RES and RT for 8 weeks ameliorates the memory-impairing effects of AC. [ABSTRACT FROM AUTHOR]

Objective: Arsenic (As) poisoning is a worldwide public health problem. Arsenic can cause cancer, diabetes, hepatic problems, etc. Hence, we investigated possible hepatoprotective properties of curcumin against As3+-induced liver damages in freshly isolated rat hepatocytes. Materials and Methods: Isolation of hepatocytes was done by the two-step liver perfusion method using collagenase. The EC50 concentration of As3+ was used in toxicity assessments and curcumin (2, 5, and 10 µM) was added 15 min before As3+ addition to isolated hepatocytes. Curcumin impact was assessed in terms of cytotoxicity, lipid peroxidation induction, reactive oxygen species (ROS) levels, and mitochondrial membrane potential. Results: As3+ significantly increased cytotoxicity, malondialdehyde and ROS levels and induced mitochondrial membrane damage and hepatocyte membrane lysis after 3 hr incubation. Curcumin 2 µM significantly prevented lipid peroxidation induction, ROS formation, and mitochondrial membrane damage; while curcumin 5 µM had no apparent effect on these parameters, curcumin 10 µM potentiated them. Conclusion: Curcumin only at low doses could ameliorate oxidative stress injury induced by As3+ in isolated rat hepatocytes. [ABSTRACT FROM AUTHOR]

The article highlights a study on the protective effects of nicotine and O-acetyl-L-carnitine against H89-induced spatial memory deficits. It discusses that the potential synergistic effects of nicotine and O-acetyl-L-carnitine in preventing protein kinase AII inhibitor (H-89)-induced spatial learning impairments.

Objective: Gallic acid (GA) is an organic acid that possesses antiinflammatory effects as it inhibits the production of metalloproteinases, tissue plasminogen activator, growth factors and adhesion molecules. Since formation of abdominal surgeryinduced adhesion bands is accompanied by inflammation, angiogenesis and cell proliferation, in the current study, we assessed potential beneficial properties of GA against adhesion bands formation in rats. Materials and Methods: Thirty-six adult male rats were assigned into six groups of six animals. After induction of anesthesia, peritoneal injury was induced using a standard method and animals received either GA (10, 25, 50 and 100 mg/kg), or normal saline, while a group of rats remained intact. Seven days after the surgery, animals were decapitated and samples were collected for pathology evaluations. Also, lipid peroxidation (TBARS) and tumor necrosis factor alpha (TNF-a) levels were determined in serum samples. Results: Our results showed that GA significantly reduced lipid peroxidation in serum samples but had no effect on TNF-a levels. Furthermore, microscopic and macroscopic injuries reduced significantly in GA-treated animals. Conclusion: Since GA reduced adhesion bands formation at microscopic and macroscopic levels, it could be considered a treatment against adhesion bands formation. [ABSTRACT FROM AUTHOR]

Since early 2020, COVID-19 has wreaked havoc in many societies around the world. As of the present, the SARS-CoV-2-borne disease is propagating in almost all countries, affecting hundreds of thousands of people in an unprecedented way. As the name suggests, the novel coronavirus, widely known as SARS-CoV-2, is a new emerging human pathogen. A novel disease of relatively unknown origin, COVID-19 does not seem to be amenable to the currently available medicines since there is no specific cure for the disease. In the absence of any vaccine or effective antiviral medication, we have no tools at our disposal, but the method of quarantine, be it domestic or institutional, to hinder any further progression of this outbreak. However, there is a record of physicians in the past who practiced convalescent blood transfusion. To their awe, the method seemed to be useful. It is anticipated that these contemporary methods will outdo any other vaccination process in the time being, as blood transfusion is instead a cost-effective and time-friendly technique. Following a successful trial, this new approach of contemporary nature to a viral disease may serve as an emergency intervention to intercept infectious outbreaks and prevent an impending epidemic/pandemic. In this review, we document the most recent evidence regarding the efficiency of convalescent plasma and serum therapy on SARS, MERS, and particularly COVID-19, while discussing potential advantages and possible risks of such practice. [ABSTRACT FROM AUTHOR]

Objective(s): The optimal formulation of Nanostructured lipid carriers (NLCs) that contains argan oil and caffeine was considered to be developed as a topical treatment for hair loss. Materials and Methods: 26 batches were prepared according to the central composite design. Dynamic light scattering technique showed size, polydispersity index (PDI), and zeta potential, and electron microscopy depicted the morphology of NLCs. Caffeine encapsulation efficiency (EE) was measured by UV/Vis spectroscopy. Fourier-transform infrared spectroscopy (FTIR) was applied to show caffeine and NLCs interactions. The caffeine invivo morin model was designed to determine the caffeine penetration into follicles and stratum corneum. Results: The optimal formulation consisted of 2% lipid, 2% surfactant, stearic acid/argan oil ratio of 3.5, and span/tween ratio of 1.25. Its spherical NLCs size, PDI, and zeta potential were 256.2 nm, 0.225, and -25.4 respectively. The caffeine EE% was 89% which was homogenously encapsulated in NLCs as shown in FTIR analysis. In vivo studies showed these nanoparticles have the ability to accumulate in the hair follicles by the time. Conclusion: The NLC formulation optimized in this study is a potential formulation for intrafollicular delivery of caffeine. [ABSTRACT FROM AUTHOR]

Copyright of Farmacia is the property of Societatea de Stiinte Farmaceutice Romania and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Carbon monoxide (CO) has been shown to induce several cardiovascular abnormalities, as well as necrosis, apoptosis and oxidative stress in the brain. Magnesium sulfate (MS) has been shown to have beneficial activities against hypoxia in the brain. In the present study, the possible protective effects of MS against CO-induced cerebral ischemia were investigated. For this purpose, 25 male Wistar rats were exposed to 3,000 ppm CO for 1 h. The animals were divided into 5 groups (n=5 in each group) as follows: The negative control group (not exposed to CO), the positive control group (CO exposed and treated with normal saline), and 3 groups of CO-exposed rats treated with MS (75, 150 and 300 mg/kg/day) administered intraperitoneally for 5 consecutive days. On the 5th day, the animals were sacrificed and the brains were harvested for the evaluation of necrosis, apoptosis and oxidative stress. Histopathological evaluation revealed that MS reduced the number and intensity of necrotic insults. The Bax/Bcl2 ratio and malondialdehyde (MDA) levels were significantly decreased in a dose-dependent manner in the MS-treated rats compared to the positive control group, while a significant dose-dependent increase in Akt expression, a pro-survival protein, was observed. In addition, MS administration reduced pro-apoptotic indice levels, ameliorated histological insults, favorably modulated oxidative status and increased Akt expression levels, indicating a possible neuroprotective effect in the case of CO poisoning. On the whole, the findings of this study indicate that MS may prove to be useful in protecting against CO-induced cerebral injury. [ABSTRACT FROM AUTHOR]

Paraquat is extensively used as a strong nitrogen-based herbicide for controlling weeds in agriculture. This herbicide is extremely toxic to humans and induces multiorgan failure due to accumulation in the cells. So far, many instances of fatal poisoning have been reported. Paraquat is metabolized primarily in the liver. Accordingly, the effects of aquatic Levisticum officinale extract on biochemical factors and oxidative status were evaluated in hepatocytes exposed to paraquat in this study. The results showed that paraquat-induced hepatocyte destruction is mediated by reactive oxygen species (ROS) production. The aquatic extracts of Levisticum officinale (100, 200, and 300µg/mL) could prevent lipid peroxidation and reduction in the potential of mitochondrial membranes (P<0.05). The antioxidants, ROS scavengers (mannitol, dimethyl sulfoxide, and a-tocopherol), and mitochondrial permeability transition pore-sealing agent (carnitine) inhibited the effects of paraquat. The pore-sealing compound inhibited hepatotoxicity, indicating that paraquat induces cell death via mitochondrial pathways. Hepatic cell death due to paraquat could be prevented by hepatocyte pretreatment with aquatic Levisticum officinale extracts, antioxidants, and ROS scavengers; therefore, oxidative stress might directly reduce the mitochondrial membrane potential. In conclusion, paraquat hepatotoxicity may be associated with oxidative stress and maintained by the disruption of mitochondrial membrane potential. Levisticum officinale aquatic extract, presumably due to its strong antioxidant properties, could protect against the destructive effects of paraquat on rat hepatocytes. [ABSTRACT FROM AUTHOR]

ABSTRACT Vanadium toxicity is a challenging problem to human and animal health with no entirely understanding cytotoxic mechanisms. Previous studies in vanadium toxicity showed involvement of oxidative stress in isolated liver hepatocytes and mitochondria via increasing of ROS formation, release of cytochrome c and ATP depletion after incubation with different concentrations (25-200 µ M). Therefore, we aimed to investigate the protective effects of Sesamum indicum seed extract (100-300 μg/mL) against oxidative stress induced by vanadium on isolated rat hepatocytes. Our results showed that quite similar to Alpha-tocopherol (100 µ M), different concentrations of extract (100-300 μg/mL) protected the isolated hepatocyte against all oxidative stress/cytotoxicity markers induced by vanadium in including cell lysis, ROS generation, mitochondrial membrane potential decrease and lysosomal membrane damage. Besides, vanadium induced mitochondrial/lysosomal toxic interaction and vanadium reductive activation mediated by glutathione in vanadium toxicity was significantly ( P < 0.05) ameliorated by Sesamum indicum extracts. These findings suggested a hepato-protective role for extracts against liver injury resulted from vanadium toxicity. © 2015 Wiley Periodicals, Inc. Environ Toxicol 31: 979-985, 2016. [ABSTRACT FROM AUTHOR]

1. 5-Fluorouracil (5-FU) and its prodrug capecitabine are key chemotherapeutic agents in the treatment of many gastrointestinal tract adenocarcinomas. In addition to their beneficial antitumor effects, they also possess undesired cardiac toxicity. In the present study, we investigated the cytotoxic mechanisms of 5-FU and capecitabine in freshly isolated rat cardiomyocytes. 2. 5-FU and capecitabine cytotoxicities were associated with reactive oxygen species (ROS) formation, lipid peroxidation and rapid glutathione depletion. Increased intracellular ROS could target mitochondria, and our findings confirmed that the cardiomyocytes mitochondrial membrane potential (ΔΨm) was rapidly decreased by 5-FU and capecitabine. Mitochondrial dysfunction subsequently initiates downstream events that trigger caspase-3 activation, and our results showed that 5-FU and capecitabine activated caspase-3 which leads to apoptosis or necrosis. However, 5-FU acted much more powerful than capecitabine at inducing several cytotoxicity markers in heart cardiomyocytes. In addition, 5-FU but not capecitabine caused lysosomal membrane leakiness when it was incubated with cardiomyocytes. All cytotoxicity markers were prevented by antioxidants, ROS scavengers, mitochondrial permeability transition (MPT) pore sealing agents and lysosomotropic agents. 3. Our findings showed that the cytotoxic action of 5-FU and capecitabine on cardiomyocytes are mediated by oxidative stress and subsequent mitochondrial dysfunction which causes caspase-3 activation and cell death. [ABSTRACT FROM AUTHOR]

This study was conducted to evaluate the cytoprotection of various extracts and bioactive compounds found in Pistacia vera againts cytotoxicity, ROS formation, lipid peroxidation, protein carbonylation, mitochondrial and lysosomal membrane damages in cell toxicity models of diabetes related carbonyl (glyoxal) and oxidative stress (hydroperoxide). Methanol, water and ethyl acetate were used to prepare crude pistachios extracts, which were then used to screen for in-vitro cytoprotection of freshly isolated rat hepatocytes against these toxins. The order of protection by Pistacia vera extracts against both hydroperoxide induced oxidative stress (ROS formation) and glyoxal induced protein carbonylation was: pistachio methanolic extract > pistachio water extract, gallic acid, catechin > α-tochoferol and pistachio ethyl acetate extract. Finally due to higher protection achieved by methanolic extract even compared to sole pretreatment of gallic acid, catechin or α-tochoferol, we suggest that cytoprotection depends on the variety of polar and non-polar compounds found in methanolic extract, it is likely that multiple cytoprotective mechanisms are acting against oxidative and carbonyl induced cytotoxicity. To our knowledge, we are the first to report the cytoprotective activity of Pistacia vera extracts against oxidative and carbonyl stress seen in type 2 diabetes hepatocytes model. [ABSTRACT FROM AUTHOR]

Harmful algal blooms produced by the marine ichthyotoxic dinoflagellateCochlodinium polykrikoidesare responsible for mass mortalities of wild and farmed fish globally. This study compared the cytotoxic mechanisms ofC. polykrikoidestotal extract on both trout and rat liver hepatocytes. Trout hepatocytes were more sensitive than rat hepatocytes againstC. polykrikoidesextract. The effective concentration 50 after 3 hour incubation (EC503hr) concentrations found forC. polykrikoidesextract in trout and rat hepatocytes (i.e., 50% membrane lysis in 3 hr) were Eq. 1 cell/ml and Eq. 240 cell/ml, respectively.C. polykrikoidesextract exposure in both isolated trout and rat hepatocytes resulted in membrane lysis, reactive oxygen species formation, glutathione depletion, collapse of mitochondrial membrane potential, ATP depletion, increase in adenosine diphosphate (ADP)/adenosine triphosphate (ATP) ratio, cytochrome c release into the hepatocyte cytosol, and activation of caspases cascade. Trout hepatocyte toxicity was also associated with lysosomal membrane injury. Mitochondrial permeability transition in both trout and rat hepatocytes produced cytochrome c release from the mitochondrial intramembrane space into the cytosol. Thus, the cytochrome c release triggered activation of caspase-3 and apoptosis. Finally, data demonstrated thatC. polykrikoidesextract may induce more apoptotic phenotype in rat than trout hepatocytes, which in the latter favored predominantly necrotic mode of cell death. [ABSTRACT FROM PUBLISHER]

In this research, we investigatedthe cytotoxic mechanisms of Cochlodinium polykrikoidescell lysate on isolated rat liver hepatocytes. This micro algae is responsible for a severe and widespread harmful algal bloom in the Persian Gulf and Gulf of Oman (2008-2009). Isolated hepatocytes were obtained by collagenase perfusion of Sprague-Dawley rat liver. According to our results, incubation of algal lysate with isolated rat hepatocytescaused hepatocyte membrane lysis, reactive oxygen species (ROS) formation, glutathione depletion, collapse of mitochondrial membrane potential, ATP depletion and increase in ADP/ATP ratio, cytochrome c release in to the hepatocyte cytosol, activation of caspase-3 (final mediator of apoptosis) and appearance of apoptosis phenotype. On the other hand, pre-treatment of antioxidants (α-tocopherol succinate and BHT), radical scavengers (mannitol and DMSO), mitochondrial permeability transition (MPT) pore sealing agents (cyclosporine A, carnitine and trifluoperazine), NADPH P450 reductase inhibitor (Diphenyliodonium chloride), CYP2E1 inhibitors (Phenylimidazole and 4-Methylpyrazole) and ATP generators (L-glutamine, Fructose and Xylitol)inhibitedcaspase-3 activation and cell death in algal lysate treated hepatocytes.Our data also confirmed that algal lysate activates apoptosis signaling via oxidative stress and mitochondrial pathway. Thus, ROS formation caused by the lysate exposure could directly be involved in mitochondrial MPT pore opening and activation of caspase-3 leading to C.polykrikoides lysateinduced apoptosis on rat hepatocytes. These findings contribute to a better understanding of C.polykrikoides-toxic effects on mammalian liver cells. [ABSTRACT FROM AUTHOR]

In this research, we investigated the cytotoxic mechanisms of one of the widely used pharmaceuticals that are regularly associated with the adverse effects on the liver, sometimes leading to acute liver failure, diclofenac. Diclofenac liver cytotoxicity was associated with reactive oxygen species (ROS) formation and lipid peroxidation which were inhibited by antioxidants and ROS scavengers, ferric chelator, inhibitors of reduced CYP2E1 and CYP2C9, mitochondrial permeability transition (MPT) pore sealing agents and endocytosis inhibitors. Incubation of hepatocytes with diclofenac caused rapid hepatocyte glutathione (GSH) depletion which is another marker of cellular oxidative stress. Most of the diclofenac-induced GSH depletion could be attributed to the expulsion of GSSG. Diclofenac cytotoxicity was also associated with mitochondrial injury, lysosomal membrane rupture and release of digestive proteases which were prevented by antioxidants, MPT pore sealing agents, lysosomotropic agents and inhibitors of cytochrome P450 isoenzymes. These events could cause cytochrome C release from the mitochondrial intramembrane space to cytosol. The cytochrome C release could trigger activation of caspase-3 and apoptosis. We finally concluded that diclofenac hepatotoxicity is a result of metabolic activation by CYP2E1 and CYP2C9 and ROS formation, leading to a mitochondrial/lysosomal toxic cross-talk in the liver hepatocytes. [ABSTRACT FROM AUTHOR]

Objective: The present study examined effects of resistance training (RT) and resveratrol (RES) alone and together on acrylamide (AC)-induced memory impairment in rats., Materials and Methods: Animals were divided into 6 groups: (1) Control group which received normal saline intraperitoneally (ip) daily for 8 weeks; (2) Scopolamine (SCO) group which received SCO (1 mg/kg/day, ip) for 8 weeks; (3) AC group which received AC (5 mg/kg/day, ip) for 8 weeks; (4) AC + RT group which received AC (5 mg/kg/day, ip) for 8 weeks and performed RT (5 days a week for 8 weeks); (5) AC + RES group which received AC (5 mg/kg/day, ip) and RES (1 mg/kg/day, ip) for 8 weeks; and (6) AC + RT + RES group which received AC (5 mg/kg/day, ip) and RES (1 mg/kg/day, ip) for 8 weeks and performed RT (5 days a week for 8 weeks). On day 53, animal training began in the Morris Water Maze (MWM) and 24 hr after the last training, the probe test was performed., Results: RT and RES alone did not significantly affect escape latency or traveled distance increased by AC. However, concomitant RES and RT treatment significantly reduced these parameters compared to the AC group. Co-treatment with RES and RT also significantly increased the time spent in the target quadrant compared to the AC group. Lipid peroxidation was reduced in the AC+RES and AC+RT+RES groups compared to the AC group., Conclusion: It seems that daily co-treatment with RES and RT for 8 weeks ameliorates the memory-impairing effects of AC., Competing Interests: The authors have declared that there is no conflict of interest.

Vanadium toxicity is a challenging problem to human and animal health with no entirely understanding cytotoxic mechanisms. Previous studies in vanadium toxicity showed involvement of oxidative stress in isolated liver hepatocytes and mitochondria via increasing of ROS formation, release of cytochrome c and ATP depletion after incubation with different concentrations (25-200 µM). Therefore, we aimed to investigate the protective effects of Sesamum indicum seed extract (100-300 μg/mL) against oxidative stress induced by vanadium on isolated rat hepatocytes. Our results showed that quite similar to Alpha-tocopherol (100 µM), different concentrations of extract (100-300 μg/mL) protected the isolated hepatocyte against all oxidative stress/cytotoxicity markers induced by vanadium in including cell lysis, ROS generation, mitochondrial membrane potential decrease and lysosomal membrane damage. Besides, vanadium induced mitochondrial/lysosomal toxic interaction and vanadium reductive activation mediated by glutathione in vanadium toxicity was significantly (P < 0.05) ameliorated by Sesamum indicum extracts. These findings suggested a hepato-protective role for extracts against liver injury resulted from vanadium toxicity. © 2015 Wiley Periodicals, Inc. Environ Toxicol 31: 979-985, 2016., (© 2015 Wiley Periodicals, Inc.)