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  • Küçük Resim
    Öğe
    Effects of Benzo(a)pyrene and Ethanol on Morphology and Antioxidant Status and Transaminases in Rat Liver
    (2014) Emre, Mehmet Hanifi; Aktay, Göknur; Polat, Alaattin; Öztürk, Feral
    Abstract: Ethanol and benzo(a)pyrene cause an increase in lipid peroxidation either by producing the reactive oxygen species or decreasing the level of endogenous antioxidant enzymes that leads to cellular damage and cellular dysfunction. The aim of this study was to investigate both physiological and histological changes in liver tissue after administration of benzo(a)pyrene and ethanol. Male Sprague Dawley rats were divided into four groups. First group (control group). Second group treated with benzo(a)pyrene [B(a)P], third group treated with benzo(a)pyrene[B(a)P] plus ethanol (EtOH) and fourth group was given ethanol(EtOH). Superoxide dismutase (SOD), alanin aminotransferase (ALT), aspartat aminotransferase (AST), gamma-glutamyl transferase (GGT), glutathione (GSH), malondialdehyde (MDA) levels as well as histological examination were evaluated to demonstrate the liver response following administration of [B(a)P] and (EtOH) separately and together. SOD activities of the liver tissue in the experimental groups were decreased when compared to the first group. Activities of ALT, AST and GGT of the liver tissue in all experimental groups were found significantly higher than that of the first group. GSH levels of the liver tissue of the experimental groups were lower than the first group especially in fourth group. When we compared MDA levels among study groups, MDA levels of experimental groups were found significantly higher than the first group. Exposure [B(a)P] to resulted in hepatocellular changes in the periportal area and inflammatory cell infiltration . On the other hand, liver tissue in third group and fourth group, which was treated with [B(a)P] plus EtOH and EtOH alone respectively, showed seldom inflammatory cell infiltrations. [B(a)P] and EtOH administration alone or together discretely determined changes in the GSH, MDA levels and SOD ALT, AST and GGT enzyme activities in the liver tissues. Additionally, we noted [B(a)P] induced hepatocellular changes in the periportal area.
  • Küçük Resim
    Öğe
    L-Name ile hipertansif yapılan sıçanlarda kalpte iskemi-reperfüzyon sonrası kalp dokusu ksantin oksidaz aktivitesi ve malondialdehit düzeyleri
    (Ege Tıp Dergisi, 2001) Fadıloğlu, Ersin; Özyurt, Hüseyin; Erdoğan, Hasan; Emre, Mehmet Hanifi
    Öz: Bu çalışmanın amacı erkek ve dişi hipertansif sıçanlarda kalpte iskemi-reperfüzyon hasarından sonra ksantin oksidaz (XO) aktivitesinin ve malondialdehit (MDA) düzeyinin tespit saptanmasıdır. L-NAME ile kronik nitrik oksit sentetaz (NOS) inhibisyonu hipertansiyon modeli oluşturmak için uygulandı. Erkek ve dişi sıçanlar üçer gruba ayrıldı. L-NAME çeşme suyu içinde 15 gün süre ile 100 mg/L ya da 500 mg/L olacak şekilde verildi. Kontrol grubuna sadece çeşme suyu verildi, iskemi-reperfüzyon (l/R) hasarı oluşturmak için sol ana koroner artere 7 dakika oklüzyon ve 7 dakika reperfüzyon uygulandı. Sonra kalp çıkarıldı ve -85'C'de çalışma gününe kadar saklandı. Dişi kontrol grubu XO aktivitesi erkek gruba göre anlamlı olarak artmış bulundu. Dişi sıçanlarda 100 mg L-NAME grubu XO aktivitesi kontrol grubuna göre anlamlı olarak azaldı. Erkek 100 mg L-NAME grubu MDA düzeyi diğer erkek gruplarına göre anlamlı artış gösterdi, üiş ikontrol grubu MDA düzeyi diğer dişi çalışma gruplarına göre vè ayrıca 500 mg L-NAME grubu MDA düzeyi 100 mg L-NAME grubuna göre anlamlı o/arak azalmış olarak saptandı. Düşük doz L-NAME ile hipertansiyon oluşturulan erkek sıçanlarda kalpte l/R sonrası lipit peroksidasyonda artış görülürken, diğer taraftan L-NAME ile hipertansiyon oluşturulan dişi sıçanlarda kalpte l/R sonrası lipit peroksidasyonda azalma görüldü. L-NAME ile hipertansiyon oluşturulan dişi sıçanlarda I/R sonrası XO enzim aktivitesi anlamlı bir şekilde azalmıştır. Başlık (İngilizce): Xhanthine oxidase activities and malondialdehyde levels in heart tissue after myocardial ischemia-reperfusion on rats with hypertension induced by L-Name Öz (İngilizce): The aim of this study was to investigate xanthine oxidase (OX)'enzyme activity and level of malondialdehyde (MDA) following heart ischemia-reperfüsion injury in male and female hypertensive rats. Chronic nitric oxide synthetase inhibition by L-NAME was performed to induce hypertension. Male and female rats were divided into three groups. L-NAME was given as 100 mg/L or 500 mg/L in tap water for 15 days. Only tap water was given to rats in control group. To produce ischemia-reperfüsion (I/R) injury, the left main coronary artery was occluded for 7 mm, followed by 7 min of reperfusion. Then heart was excised and had been stored at -85'C up to study day. XO activity of female control group was higher than male one. It was found that XO activity of female 100 mg L-NAME group was lower than control one. MDA level of male 100 mg L-NAME group showed remarkable increase compared to other male group. It was found that MDA level of female control group was higher than those of other female groups. On the other hand, MDA level of female 500 mg L-NAME group was significantly lower than 100 mg L-NAME one. Increased lipid peroxidatlon .was seen after myocardial I-R injury in male rats with hypertension induced by low dose L-NAME, whereas decreased lipid peroxidation was seen after myocardial I-R injury in female rats with hypertension induced by L-NAME. Hypertension induced, by low dose L-NAME caused remarkable decrease in XO enzyme activity of female rats after I/R.
  • Küçük Resim
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    Protective role of aminoguanidine on gentamicin induced acute renal failure in rats
    (Acta Histochemica, 2006) Polat, Alaadin; Parlakpınar, Hakan; Taşdemir, Seda; Çolak, Cemil; Vardı, Nigar; Uçar, Muharrem; Emre, Mehmet Hanifi; Acet, Hacı Ahmet
    The toxicity of aminoglycosides including gentamicin (GEN), the most widely used drug in this category, is believed to be related to the generation of reactive oxygen species (ROS) in the kidney. Aminoguanidine (AG) is known as an effective antioxidant and its free radical scavenger effects may protect GEN-induced acute renal failure (ARF). Therefore, this study was focused on investigating the possible protective effect of AG against GENinduced nephrotoxicity in an in vivo rat model. We investigated the effects of AG on GENinduced changes in renal tissue malondialdehyde (MDA) levels; nitric oxide (NO) generation; glutathione peroxidase (GSH-Px), superoxide dismutase (SOD), and catalase (CAT) activities; glutathione (GSH) content; serum creatinine (Cr) and blood urea nitrogen (BUN) levels. Morphological changes in the kidney were also examined using light microscopy. GEN administration to control group rats increased renal MDA and NO levels but decreased GSH-Px, SOD, CAT activities and GSH content. AG administration with GEN injection resulted in significantly decreased MDA, NO generation and increased GSH-Px, SOD, CAT activities and GSH content when compared with GEN alone. Serum levels of Cr and BUN significantly increased as a result of nephrotoxicity. Also, AG significantly decreased Cr and BUN levels. Morphological changes in the kidney, including tubular necrosis, intracellular edema, glomerular and basement membrane alterations were evaluated qualitatively. Both biochemical findings and histopathological evidence showed that administration of AG reduced the GEN-induced kidney damage. We propose that AG acts in the kidney as a potent scavenger of free radicals to prevent the toxic effects of GEN both at the biochemical and histological level.