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Search Results: 1 - 10 of 456 matches for " Jalal Pourahmad "
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The Need to Establish a Common Base Line for the Characteristics of Safety Withdrawal of Prescription Drugs from Worldwide Pharmaceutical Markets
Jalal Pourahmad
Iranian Journal of Pharmaceutical Research , 2008,
Abstract:
History of Medical Sciences in Iran
Jalal Pourahmad
Iranian Journal of Pharmaceutical Research , 2008,
Abstract: The practice and study of medicine in Persia has a long and prolific history. The ancient Iranian medicine was combined by different medical traditions from Mesopotamia, Egypt, India, China and Greece for more than 4000 years and merged to form what became the nucleus and foundation of medical practice in the European countries in the 13th century. The Iranian academic centers like Jundishapur University (3rd century AD) were a breeding ground for the union among great scientists from different civilizations. These centers successfully followed their predecessors’ theories and greatly extended their scientific research through history. Iranian physicians during the glorious Islamic civilization had a tremendous share in the progress of medical sciences. The excellent clinical observations and physical examinations and writings of Iranian scientists such as Rhazes (Al-Razi, 865-925 AD), Haly Abbas (Ali ibn-al Abbas-al Majusi, died 994 AD), Avicenna (Abou Ali Sina, 980-1037) and Jurjan (Osmail ibn al-Husayn al-Jurjani, 110 AD) influenced all fields of medicine The new era of medicine in Iran begins with establishment of Dar-ul-funoon in 1851, which was the only center for modern medical education before the establishment of Tehran University. Following the establishment of the Tehran university school of medicine in 1934 and the return of Iranian graduates from the medical schools in Europe, much progress was made in the development and availability of trained manpower and specialized faculties in medicine. After the Islamic revolution by the growing spirit of independence inspired by the Iranian government the number of medical schools and medical students increased more than 10 times. For the 1st time in recent modern history the Iranian medical universities started to offer post-graduate specialized degrees in basic, clinical and engineering sciences.
Identification of Intracellular Sources Responsible for Endogenous Reactive Oxygen Species Formation
Jalal Pourahmad
Iranian Journal of Pharmaceutical Research , 2002,
Abstract: The endogenous reactive oxygen species ( ROS ) formation is associated with many pathologic states such as inflammatory diseases, neurodegenerative diseases, brain and heart ischemic injuries, cancer, and aging. The purpose of this study was to investigate the endogenous sources for ROS formation in intact isolated rat hepatocytes, in particular, peroxisomal oxidases, monoamine oxidase, xanthine oxidase, cytochrome P450, and mitochondria electron transport. The rat hepatocyte cat alyzed oxidation of 2’,7’- dichlorofluorescin to form the fluorescent 2,7’-dichlorofluorescein was used to measure endogenous and xenobiotic-induced reactive oxygen speci es ( ROS ) formation by intactisolated rat hepatocytes. Various oxidase substrates and inhibitors were then used to identify the intracellular oxidases responsible. Endogenous ROS formation was markedly increased in catalase inhibited or GSH depleted hepatocytes, and was inhibited by ROS scavengers or des feroxamine. Endogenous ROS formation was also inhibited by cytochrome P450 inhibitors, but was not affected by oxypurinol, a xanthine oxidase inhibitor. Mitochondrial respiratory chain inhibitors or hypoxia, on the other hand, markedly increased ROS before cytotoxicity ensued. This suggests endogenous ROS formation can largely be attributed to oxygen reduction by reduced mitochondrial el ectron transport components and reducedcytochrome P450 isozymes. Addition of monoamine oxidase substrat es increased antimycin Aresistant respiration and ROS formation before cytotoxicity ensued. On the other hand peroxisomal substrates readily induced ROS formation and were cytotoxic towards catalaseinhibited hepatocytes, which suggests that peroxisomal catalase removes endogenous H2O2 formed in the peroxisomes. The consequences of upregulation of peroxisomal oxidases are discussed.
Vanadium induces liver toxicity through reductive activation by glutathione and mitochondrial dysfunction  [PDF]
Mir-Jamal Hosseini, Nina Seyedrazi, Jafar Shahraki, Jalal Pourahmad
Advances in Bioscience and Biotechnology (ABB) , 2012, DOI: 10.4236/abb.2012.38134
Abstract: Pentavalent vanadium (V5+) (metavanadate salt) tox- icity is a challenging problem to the health professionals and has been recognized as an industrial hazard that adversely affects human and animal health, but its cytotoxic mechanisms have not yet been completely understood. In this study, we investigated the cytotoxic mechanisms of V5+ in freshly isolated rat hepatocytes. V5+ cytotoxicity was associated with reactive oxygen species (ROS) formation, collapse of mitochondrial membrane potential, lysosomal membrane rupture and cytochrome c release into the hepatocyte cytosol. All of the above mentioned V5+ -induced cytotoxicity markers were significantly (p < 0.05) prevented by ROS scavengers, antioxidants and mitochondrial permeability transition (MPT) pore sealing agents. Hepatocyte glutathione (GSH) was also rapidly oxidized and GSH-depleted hepatocytes were more resistant to lithium-induced oxidative stress markers. This suggests that V5+ is activated by GSH. Our findings also showed that the lysosomotropic agents prevented V5+ induced mitochondrial membrane potential collapse. On the other hand, mitochondrial MPT pore sealing agents inhibited lysosomal membrane damage caused by V5+. It can therefore be suggested that there is probably a toxic interaction (cross-talk) between mitochondrial and lysosomal oxidative stress generating systems, which potentiates ROS formation and further damages both sub-organelles in V5+-induced induced hepatotoxicity. In conclusion, V5+-induced cytotoxicity can be attributed to oxidative stress started from glutathione mediated metal reductive activation and continued by mitochondrial/lysosomal toxic interaction.
Application of Cell-Based Assay Systems for the Early Screening of Human Drug Hepatotoxicity in the Discovery Phase of Drug Development
Jalal Pourahmad,Peter J O’Brien,Parivash Eftekhari
Iranian Journal of Pharmaceutical Research , 2005,
Abstract: While drug toxicity (especially hepatotoxicity) is the most frequent reason cited for withdrawal of an approved drug, no simple solution exists to adequately predict such adverse events. Simple cytotoxicity assays in HepG2 cells are relatively insensitive to human hepatotoxic drugs in a retrospective analysis of marketed pharmaceuticals. In comparison, a panel of pre-lethal mechanistic cellular assays hold the promise to deliver a more sensitiveapproach to detect endpoint-specific drug toxicities. The panel of assays covered by this review includes steatosis, cholestasis, phospholipidosis, reactive intermediates, mitochondria membrane function, oxidative stress, and drug interactions. In addition, the use of metabolically competent cells or the introduction of major human hepatocytes in these in-vitro studies allow a more complete picture of potential drug side effect. Since inter-individual therapeutic index (TI) may differ from patient to patient, the rational use of one or more of these cellular assay and targeted in-vivo exposure data may allow pharmaceutical scientists to select drugcandidates with a higher TI potential in the drug discovery phase.
Influx and Efflux of Glutathione During Continuous Pain Induction in Rat Hepatocytes and Glial Cells
Jalal Pourahmad,Niloofar Rezvani,Mohsen Rezaei,Abolhasan Ahmadiani
International Journal of Pharmacology , 2006,
Abstract: In this study we examined the intra and extracellular glutathione levels in both glial cells and hepatocytes of rats during continuous pain induction. Animals were divided in 4 groups; one day, four day and seven day pain groups vs. control group. Results showed that the maximum generation of ROS occurs in four day group of continuous pain induction in both glia and hepatocytes of rats. The intracellular GSH was at highest level in one day pain group due to GSH influx and synthesis as two defensive mechanisms against oxidative stress in both glia and hepatocytes. In hepatocytes, however, by considering the levels of extracellular GSSG in one day pain group, it seems that the enzymatic function of GSSG reductase is also another important defense mechanism in the first group of continuous pain induction. Maximum extra cellular GSSG was in 7 day pain group in both glia and hepatocytes. Results suggest that following continuous pain induction, oxidative stress is the major cause for GSH depletion in both glia and hepatocytes and leads cells to the later consequences including apoptosis.
On the Zeros of Daubechies Orthogonal and Biorthogonal Wavelets  [PDF]
Jalal Karam
Applied Mathematics (AM) , 2012, DOI: 10.4236/am.2012.37116
Abstract: In the last decade, Daubechies’ wavelets have been successfully used in many signal processing paradigms. The construction of these wavelets via two channel perfect reconstruction filter bank requires the identification of necessary conditions that the coefficients of the filters and the roots of binomial polynomials associated with them should exhibit. In this paper, orthogonal and Biorthogonal Daubechies families of wavelets are considered and their filters are derived. In particular, the Biorthogonal wavelets Bior3.5, Bior3.9 and Bior6.8 are examined and the zeros distribution of their polynomials associated filters are located. We also examine the locations of these zeros of the filters associated with the two orthogonal wavelets db6 and db8.
Using Transposon Mutagenesis to Find an Alternative Resolvase in an Escherichia coli Cells Lacking RuvABC
Razieh Pourahmad Jaktaji
Pakistan Journal of Biological Sciences , 2009,
Abstract: This study was undertaken to identify an unknown resolvase in an E. coli strain lacking RuvABC (N4237) by using transposon mutagenesis. One out of 10000 clones was retained for further study as it was resistant to UV light and mitomycin C. The result of transductional mapping and PCR sequencing showed that Tn10kan inserted upstream of rusA gene and expression of this gene improved survival. Thus, results did not show the presence of new resolvase in E. coli cells.
"Involvement of metabolic reactive intermediate Cr (IV) in Chromium (VI) cytotoxic effects "
Pourahmad J,O’Brien PJ
DARU : Journal of Pharmaceutical Sciences , 2001,
Abstract: Addition of Cr VI (dichromate) to isolated rat hepatocytes results in rapid glutathione oxidation, reactive oxygen species (ROS) formation, lipid peroxidation, decreased mitochondrial membrane potential and lysosomal membrane rupture before hepatocyte lysis occurred. Cytotoxicity was prevented by ROS scavengers, antioxidants, and glutamine (ATP generator). Hepatocyte dichlorofluorescin oxidation to dichlorofluorescein (DCF) to determine ROS formation was inhibited by mannitol (a hydroxyl radical scavenger) or butylated hydroxyanisole and butylated hydroxytoluene (antioxidants). The Cr VI reductive mechanism required for toxicity is not known. Cytochrome P450 inhibitors, Particularly CYP 2E1 inhibitors, but not inhibitors of DT diaphorase or glutathione reductase also prevented cytotoxicity. This suggests that P450 reductase and/or reduced cytochrome P450 contributes to Cr VI reduction to Cr IV. Glutathione depleted hepatocytes were resistant to Cr (VI) toxicity and much less dichlorofluorescin oxidation occurred. Reduction of dichromate by glutathione or cysteine in vitro was also accompanied by oxygen uptake and was inhibited by Mn II (a Cr IV reductant). Cr VI induced cytotoxicity and ROS formation was also inhibited by Mn II, which suggests that, Cr IV and Cr IV GSH mediate "ROS" formation in isolated hepatocytes. In conclusion Cr VI cytotoxicity is associated with mitochondrial/lysosomal toxicity by the metabolic reactive intermediate Cr IV and “ROS”.
Peculiarities of CO2 exchange in soybean genotypes contrasting in grain yield  [PDF]
Jalal A. Aliyev
Advances in Biological Chemistry (ABC) , 2012, DOI: 10.4236/abc.2012.23039
Abstract: The peculiarities of leaf carbon dioxide gas exchange in soybean genotypes grown in field over a large area and contrasting in duration of vegetation, photosynthetic traits and productivity were studied. Varietal differences in the daily and ontogenetic changes in photosynthesis and photorespiration were identified. It was established that the period of the high activity of photosynthetic apparatus in high productive soybean genotypes lasts for a longer time. The photosynthetic rate and the rate of CO2 release in light due to photorespiration are higher in high productive genotypes. A value of photorespiration in contrasting soybean genotypes constitutes about 28% - 35% of photosynthetic rate. The ratio of gross photosynthesis to photorespiration in genotypes with different productivity is constant enough during ontogenesis, indicating a direct positive correlation between gross photosynthesis and photorespiration. Therefore, contrary to conception arisen during many years on the waste-fulness of photorespiration, taking into account the versatile investigations on different aspects of photo-respiration, it was proved that photorespiration is one of the evolutionarily developed vital metabolic processes in plants and the attempts to reduce this process with the purpose of increasing the crop productivity are inconsistent.
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