Free radical production related with many stress factors including radiation, drugs, ageing and trauma plays a key role in cell death. Notwithstanding, free radicals can cause pathology in a variety of diseases through oxidative stress Under oxidative stress, excessive production of free radicals can trigger cell death by primarily DNA and all cellular macromolecule damages. Also, excessive free radicals have a role in early inducers of autophagy cell death upon nutrient deprivation. Autophagy is physiologic process of eukaryotic systems, which have signiicant role in adaptation to oxidative stress by degradation of metalloproteins and oxidatively damaged macromolecules. By oxidizing, membrane injuries allow the leakage of enzymes and contribute to cell damage. However, recent publications demonstrate the protecting role of lysosome system during excessive reactive oxygen species ROS production by the elimination of damaged proteins or organelles. Activation of autophagic or lysosomal system can eliminate the oxidizing components of cell in oxidative stress response. This chapter aims to provide the novel insight data for oxidative damage-mediated autophagy as well as their metabolic networks.
Background: Obesity is a worldwide health problem and causes many important illnesses. The current study aimed to investigate the influence of quercetin over apoptosis by inflammatory activity on high-fat dietinduced liver damage. Material and methods: Totally 18 adult female Sprague-Dawley rats were selected and randomly separated equally into three groups, followed as control, obesity and obesity-quercetin groups. Obesity and obesityquercetin groups were fed a moderately high fat diet for 120 days. After obesity occurred, quercetin dissolved in the corn oil and given obesity-quercetin group at dose of 50 mg/kg by oral gastric way for 15 days. All animals were sacrificed with an anesthesia at the end of the experiment, and venous blood samples were collected from the right ventricle and hepatic markers were evaluated by using commercially available diagnostic kits. In addition, liver sections were analysed by histopathologic and immunohistochemical procedures. Also, we evaluated the expression of Bax and Bcl-2 by immunohistochemistry. Results: Obesity induced important change (p<0.05) in the most of biochemical parameters, hepatic markers, and Bax immunoreactivity as well. But, the level of Bcl-2 was slightly increased, in contrast, the level of Bax decreased markedly (p<0.05) in the obesity-quercetin group. Conclusions: Both immunohistochemical evidence and biochemical results showed that application of quercetin decreased the obesity mediated damage to the liver.
Vücuda çeşitli hasarlar veren stres faktörlerine karşı organizmada yanıt oluşturan yapıların başında nöroendokrin sistemin geldiği bilinmektedir. Biz de sıçanlarda kronik stres modeliyle adrenal bezlerde oluşabilecek morfolojik ve histolojik değişiklikleri araştırmayı amaçladık. Gereç ve Yöntemler: 24 Sprague Dawley sıçan, her birinde 6'şar erkek veya dişi sıçan olan 4 gruba ayrıldı. 14 gün, dişi ve erkek kontrol gruplarına hiçbir uygulama yapılmazken, stres gruplarına kronik stres prosedürü uygulandı. Sıçanların ağırlıkları 3 kez tartıldı. Fiksasyondan sonra rutin histolojik işlemlerden geçirilen adrenal bezler parafine gömüldü. Alınan kesitler Hematoksilen-Eozin, PAS ve Masson Trikrom yöntemleriyle boyanarak histopatolojik açıdan incelendi. Mikrometrik okülerle kesitlerin morfometrik değerlendirmesi yapılarak tüm ölçüm sonuçlarının istatistiksel analizleri gerçekleştirildi. Bulgular: Dişi stres grubunun ağırlığı kontrole kıyasla anlamlı derecede azalırken, erkek stres grubundaki ağırlık artışı kontrol grubuna kıyasla anlamlı bulunmadı. Ayrıca hem dişi hem de erkek stres gruplarının korteks kalınlığında, kendi kontrollerine kıyasla anlamlı bir artış mevcuttu. Stres gruplarının adrenal bezlerinde nükleer ve sitoplazmik dejenerasyonlar, adrenokortikal hiperplazi, makrofajlar, sinüzoidlerde dilatasyon ve bağ dokusunda artış gözlendi. Sonuç: Kronik stres dişilerde kilo kaybına, erkek ve dişilerde kortekste kalınlaşmaya ve hücresel dejenerasyonlara sebep olabilmektedir.
ÖzetAmaç: Günlük yaşamın bir parçası haline gelen stres, vücudun dengesini bozarak pek çok hastalığa neden olur. Biz de bu çalışmada, kronik strese sebep olan faktörlere maruz kalındığında böbrekte meydana gelebilecek olası yapısal değişiklikleri araştırmayı amaçladık.Yöntem: Bu çalışmada 12 adet Sprague Dawley cinsi yetişkin erkek sıçan kullanıldı. Sıçanlar rastgele kontrol (n=6) ve stres (n=6) grubu olarak ikiye ayrıldıktan sonra, stres grubundakilere 4 hafta boyunca "beklenmedik kronik hafi f stres" protokolü uygulandı. Deneyin sonunda anestezisi altında feda edilen bütün sıçanların böbrekleri çıkarıldı ve derhal "suya daldırma yöntemi" ile hacimleri ölçüldü. Böbrekler rutin histolojik işlemleri takiben, histopatolojik değerlendirme için ışık mikroskobunda incelendi.Bulgular: Stres grubundaki sıçanların böbrek hacimlerinin (0,90 ± 0,096 ml) kontrol grubundakilerin böbrek hacimlerine (1,075 ± 0,106 ml) kıyasla önemli düzeyde azalmış olduğu (p<0,05; independent samples t test) tespit edildi. AbstractObjective: Stress, which is a part of daily life, causes many diseases by disrupting the existing balance in the body. In this study, we aimed to investigate possible renal structural changes resulting from the exposing to chronic stress-producing factors.Method: Twelve male, adult Sprague Dawley rats were used in this study. After the rats were divided into two groups as the control (n=6) and stress (n=6) groups, unpredictable chronic mild stress (CMS) protocol was applied to the stress group for 4 weeks. At the end of the experiment, the kidneys were removed from the sacrifi ced rats under the anaesthesia, and promptly, renal volumes were measured by using the water immersion method. After a routine histological procedure, the kidneys were examined under a light microscope for histopathological evaluations.Results: When comparing with the control kidney volumes (1.075 ± 0.106 ml), the kidney volumes of the stress group (0.90 ± 0.096 ml) were found signifi cantly lower (p<0.05, independent samples t test). At the light microscopic examination of the stress kidneys, necrotic degeneration and epithelial desquamation of the nephron tubules were determined. Cytoplasmic swelling and cellular vacuolizations, leading to cellular lysis and disruption of the tubular wall integrity, were evident in the proximal and distal tubule epithelia. Necrotic alterations of the epithelium and luminal dilatations were also prominent in the loop of Henle. Additionally, glomerular shrinkage and an enlargement of Bowman's space were observed.Conclusion: On the basis of our fi ndings, it has thought that chronic stress causes to glomerular damage and epithelial cell injury of nephron tubules, leading most probably to functional impairment of kidney. ( Sakarya Med J 2017, 7(4):168-175)
Cyclophosphamide (CYP), an anticarcinogenic agent, is widely used in the chemotherapy. At high doses of the CYP causes fatal cardiomyopathy with acute cardiotoxicity. Our aim in this study investigations effects of quercetin (Q) on CYP-induced cardiotoxicity. In the present study used fifty piece Sprague Dawley male (250 ± 50 gr) rats. Rats were divided randomly to five group (n = 10). The control group was given intragastric (ig) corn oil (1 ml) for seven days. The CYP group rats were applicate ig corn oil for seven days and injected intraperitoneal (ip) a single dose of CYP 200 mg/kg on the seventh day. The groups Q50 + CYP and Q100 + CYP, respectively, were given Q in doses of 50 and 100 mg/kg dissolved in corn oil and administered ig for seven days. In addition, these groups were given single dose of CYP (200 mg/kg, ip) on the seventh days of application Q. The Q100 group was given Q (100 mg/kg-i.g) for seven days. In the end experimental applications, the blood was collected from anesthetized rats and rats were sacrificed. Serum was separated by centrifugation and utilized for the evaluation of various cardiac enzymes (CK, CK-MB, LDH, AST, ALT). The cardiac tissues used for biochemical and histopathological analysis. The data were analyzed by Tukey test in the one-way ANOVA. When data are showed compared among groups from the point of view aortic and vascular tissues, MDA level was significantly higher in the CYP group compared with control group, and determined to be decreased in CYP + Q100 group. SOD and GSH levels were significantly decreased in the CYP group compared to the control and CYP + Q100 groups. AST, CK, CK-MB, ALT and LDH levels in the serum were significantly increased in the CYP group compared with the other groups. The histopathological examination of cardiac tissue determined in the CYP group had significantly degenerated cells and cardiac myofibril. Intensity of terminal deoxynucleotidyl transferase (TdT) dUTP Nick-End Labeling (TUNEL) and beta-myosin heavy chain (β-MHC) positivity was higher in the CYP group sections compared to the control and CYP + Q100 groups sections. Both biochemical results and immunohistochemical evidence showed that Q has protective effects on CYP-induced cardiotoxicity.
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