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Öğe Effects of acetylsalicylic acid on rats: An in vivo experimental study in azaserine-rat model(Wolters Kluwer Medknow Publications, 2019) Yildiz, Hasan; Kalipci, Erkan; Oztas, Haydar; Yildiz, DenizAim: The effect of acetylsalicylic acid (ASA) on thiol levels was studied in a rat model of azaserine carcinogenesis. Materials and Methods: ASA and azaserine were applied to the animals to research changes in cellular sulfhydryl (-SH) content and variations in free and protein-bound molecules containing the -SH group. Such effects in rats injected with azaserine were investigated at low (200 ppm) and high (400 ppm) concentrations of ASA over a relatively short (6 months) and a relatively long (12 months) period. Results: Changes in the hepatic, pancreatic, and renal -SH contents were also determined. Conclusion: Compared to the other tissues studied, the liver contained the highest levels of both free and protein-bound -SH.Öğe Inhibition Effects of Acetylsalicylic Acid with Nitric Oxide (NO-ASA) on Neoplastic Changes in the Exocrine Pancreas Acinar Cells of the Azaserine Injected Rats(Discovery Medicine, 2024) Dogan, Serhat; Yildiz, HasanBackground: Atypical acinar cell foci (AACF) seen in pancreatic cancer are fatal and have been studied with some causative agents. However, for the first time, the effect of acetylsalicylic acid with nitric oxide (NO-ASA) on AACF was examined in this study. Although NO-ASA has very successful inhibitory effects against some types of cancer, it has not been investigated whether they can exert their inhibition effects on AACFs. Methods: For experimental purposes, 21 14-day-old male Wistar albino rats were used. Azaserine (30 mg/kg) was dissolved in 0.9% NaCl solution and injected intraperitoneally (i.p.) into 14 rats, except for the Control group (Cont) rats, for three weeks. Rats that were injected with azaserine once a week for three weeks and those that did not receive treatment were divided into experimental groups. 15 days after the end of the azaserine injection protocol, NO-ASA was applied to azaserine with NO-ASA (Az+NO-ASA) group rats three consecutive times with an interval of 15 days by gavage. At the end of the 5-month period, pancreatic tissue was dissected and weighed. Pancreas preparations prepared from histological sections were examined for AACF burden and analyzed via a video image analyzer. One-way analysis of variance (ANOVA) non-parametric statistical analyses were performed to test whether there was a difference between the averages of the experimental and Control groups. Results: AACF burden in both groups injected with azaserine was found to be statistically significant in all categories compared to that of the Control group (p < 0.05). The average Calculated Estimated average AACF volume (mm(3)) values, the Calculated estimated average AACF diameter (mu m), the Estimated average number of AACF per unit volume, AACF rate as a % of Calculated Organ Volume were higher in the AzCont group rats than in the Az+NO-ASA group, when compared, and there was an important level statistical difference between the groups (p < 0.05). It was determined that for all parameters AACFs load in Az+NO-ASA group rats were significantly reduced compared to that of AzCont group rats (p < 0.05). Conclusions: We observed that, as a result of the NO-ASA application, the experimental AACF focus ratio created by azaserine injection was significantly inhibited. The inhibitory effect of AACFs in Az+NO-ASA group rats may have resulted from the significant and independent chemopreventive and/or chemotherapeutic activity of NO-ASA against exocrine pancreatic AACF foci.Öğe Inhibitory effects of Aspirin on Azaserine initiated pancreatic carcinogenesis in rat(Indian Veterinary Journal, 2008) Yildiz, Hasan; Koc, Ahmet; Oztas, Haydar; Yildiz, DenizIn vitro experiments and limited animal studies suggest that aspirin, nonsteroidal anti-inflammatory, drug may inhibit pancreatic carcinogenesis. So far researchers have evaluated the biochemical and metabolic properties of aspirin but there has not been any experimental study performed on the anticarcinogenesis effect of aspirin on the well-known azaserine-rat model for pancreatic carcinogenesis. This study was designed to evaluate the potential anticarcinogenetic effect of aspirin.Öğe Investigation of Possible Ecotoxic Effects of Acrylamide on Liver with the Azaserine-Rat Model(Hard, 2012) Kalipci, Erkan; Yener, Yesim; Yildiz, Hasan; Oztas, HaydarIn this study, when acrylamide is taken into the body by nutrition, it was aimed to investigate its ecotoxic and/or carcinogenic effects on the liver. The Azaserine-Rat model developed by Longnecker and Curphey was used in this research, and in total 60 Wistar Albino race male rats were used, including 10 rats in each group. The rats were fed for 16 weeks by adding acrylamide at rates of 5 mg/kg/day and 10 mg/kg/day in drinking water. Moreover, neoplastic structures were formed by azaserine application and its effect on the development of these neoplastic structures was also investigated. As a result of this study, it was determined that ecotoxic and histopathological alterations, together with atypical cells, focuses formed in the livers of the rats in the group to which azaserine was applied and in the livers of the rats in the groups that included 5 and 10 mg/kg/day acrylamide in their drinking water. Moreover, it was found that the development (average focus diameter and focus volume) of neoplastic structures formed with azaserine was increased by 5 and 10 mg/kg/day acrylamide. These results make it possible for the probability of acrylamide to be a cancer initiator in the livers of rats.Öğe Methyl parathion-induced changes in free and protein-bound SH levels in rat tissues(Taylor & Francis Ltd, 2006) Yildiz, Deniz; Dalkilic, Semih; Yildiz, Hasan; Oztas, HaydarThe main objective of this study was to investigate the changes in free and protein-bound SH contents in methyl parathion-exposed rat tissues. The free and protein-bound SH levels are usually affected and depleted by oxidative stress-inducing agents. Results would indicate if methyl parathion toxicity partly results from depletion of sulfhydryl content of tissues. Six-week-old male Wistar albino rats were used in this study. Following exposure to methyl parathion for 3 months, the liver, the brain, and the kidney tissues were removed from the rats. The free and protein-bound SH contents were determined in these tissues. In addition, plasma lactate dehydrogenase levels were determined. Our results showed that methyl parathion exposure significantly lowers the free and protein-bound SH levels in rat tissues. However, lactate dehydrogenase activity in the blood plasma did not display any differences compared to the control group. The free SH concentrations in the control rat liver, brain, and kidney tissues were 3.78 +/- 0.1 mu mol/100 mg tissue, 1.56 +/- 0.08 mu mol/100 mg tissue, and 2.16 +/- 0.08 mu mol/100 mg tissue, respectively, whereas the free SH concentrations in rats exposed to methyl parathion were determined as 0.536 +/- 0.1 mu mol/100 mg tissue in the liver, 1.06 +/- 0.1 mu mol/100 mg tissue in the brain, and 0.108 +/- 0.03 mu mol/100 mg tissue in the kidney. The protein-bound SH concentrations in the liver and in the kidney in rats exposed to methyl parathion displayed a significant decrease also. However, the protein-bound SH level in the brain did not change significantly. These results indicate that methyl parathion exposure partially depletes the free and protein-bound SH levels. Thus, it was concluded that methyl parathion toxicity may partly result from oxidative stress.Öğe Potential neoplastic effects of parathion-methyl on rat liver(Science Press, 2009) Coral, M. Nisa Unaldi; Ucman, Sonay; Yildiz, Hasan; Oztas, Haydar; Dalkilic, SemihThe mutagenic and carcinogenic effects of parathion-methyl were examined by bacterial reverse mutation assay and a long-term experiment with wistar rats. The potential mutagenic effect of parathion-methyl in Salmonella typhimurium TA100 bacterial cells was observed without rat liver S9 metabolic activation. Parathion-methyl was further investigated for pathological changes in rat pancreas and liver. The long-term rat experiments showed that parathion-methyl exposure for 3 months can cause pathological changes in rat pancreases acinar cells and pancreatic hepatocytes. Atypical acinar cell focuses (AACF) were determined in the liver and pancreas of the rats. The results from short-term Ames test and long-term rat experiments suggested that parathion-methyl would be potential carcinogenic.
