HTK-Alcar, a modified organ transplantation solution, decreases ischemic injury in the rat kidney tissue

Objectives: Histidine-tryptophan-ketoglutarate (HTK) solution is the storage solution used in organ transplantation. However, such solutions cannot completely eliminate tissue damage. Acetyl L-carnitine (Alcar) is a strong antioxidant. In this study we aimed to determine the protective effects of HTK solution prepared with Alcar in kidney tissue. Methods: Twenty-four rats used in this study were divided into 4 groups. Kidneys of rats in groups 1 and 2 were stored for 4 hours in HTK and HTK+Alcar solutions, respectively. Kidneys of rats in groups 3 and 4 were stored for 24 hours in HTK and HTK+Alcar solutions, respectively. Histological and immunohistochemical examinations of the kidneys were performed. In addition, TUNEL analysis was performed for the evaluation of apoptosis. Results: The findings of histomorphological damage in short-term HTK and HTK+Alcar groups were mild, but it was found widely in long-term HTK and ong-term HTK+Alcar groups on histologic evaluation. When histological scoring was made from kidney sections stained with H&E, the scores in HTK+Alcar groups decreased significantly compared to HTK groups. It was also seen that the score level increased significantly in long-term groups. According to immunohistochemical evaluation, in short- and long-term HTK +Alcar groups, the acetyl-L-carnitine prevented the antiapoptotic mechanisms to be activated and the intense expression of Bcl-2 has not occurred. In short- and long-term HTK groups, osteopontin showed more immunopositive result. Conclusion: It was determined that the modified HTK solution prevented the increase of the activation of the expected oxidant mechanisms resulting in ischemia. This contribution of acetyl-L-carnitine was also found in long-term group findings. © Copyright 2020 by Gazi University Medical Faculty

Evaluation of Serum Superoxide Dismutase Activity, Malondialdehyde, and Zinc and Copper Levels in Patients With Keratoconus

WOS: 000387863300009PubMed ID: 27617869Purpose: The aim of this study was to evaluate the relationship between antioxidant superoxide dismutase (SOD) enzyme activity, malondialdehyde (MDA) as a lipid peroxidation marker, and some trace elements such as zinc (Zn) and copper (Cu) levels in patients with keratoconus. Methods: A total of 58 patients with keratoconus and 53 control subjects with similar age and sex were evaluated in this study. The modified Krumeich keratoconus classification was used to divide the patients into 4 stages. Serum SOD activity, MDA, and zinc and copper levels were compared between the patient and control groups. Results: The median serum SOD activity, MDA, and Zn and Cu levels were 27.2 (42.4-13.7) U/mL, 10.2 (11.9-8.5) nmol/mL, 87.9 (104.6-76.5) mu mol/L, and 103.2 (117.9-90.3) mu mol/L in the keratoconus group and 26.2 (32.5-14.4) U/mL, 8.8 (11.4-7.1) nmol/mL, 100.5 (121.1-81.8) mu mol/L, and 98.4 (120.3-83.4) mu mol/L in the control group, respectively. There was a statistically significant difference between the MDA and Zn levels of the keratoconus group and control subjects but not between the respective SOD activities or Cu levels (P = 0.016, P = 0.031, P = 0.440, and P = 0.376, respectively). We found no significant difference between the keratoconus group stages for serum SOD activity, serum MDA, and Zn and Cu levels (P > 0.05), and there was also no significant correlation between the keratoconus group stages and serum SOD activity, serum MDA, and Zn and Cu levels (P > 0.05). Conclusions: There is imbalance in the systemic oxidant/antioxidant status where Zn deficiency also plays a role in patients with keratoconus

Investigation of argyrophilic nucleolar organizing region

BACKGROUND: Ischemia/reperfusion (I/R) injury is a complex event frequently observed in vascular surgery and can cause functional and structural cell damage. Nucleolar-organizing regions (NORs) are sites of the ribosomal genes located on chromosomes and can be stained with silver when they are active. Thus these proteins are named as argyrophilic-NOR (AgNOR)-associated proteins. We aimed to investigate any possible effects of renal I/R injury on the NOR protein synthesis and association between the AgNOR proteins amount and histopathological injuring score

Ischemic modified albumin as a new biomarker in predicting oxidative stress in alopecia areata

Background/aim: Results show that oxidative stress is a pathophysiologic factor for alopecia areata (AA); however, the markers used can be confounding. Thus, we aimed to investigate the role of oxidative stress in the pathogenesis of AA through an evaluation of ischemia-modified albumin (IMA); other markers of the oxidant/antioxidant system, such as SOD, CAT, GSH-ST, and MDA; and contributing clinical risk factors. Materials and methods: The usefulness of IMA as a new marker for oxidative stress was compared with that of other markers and evaluated in patients with AA. Results: The mean serum level of IMA was of higher statistical significance in AA patients than in the control group (IMA: 0.57 +/- 0.01 vs. 0.52 +/- 0.02 Delta ABSU, P < 0.0001). IMA (P = 0.03, OR = 25.8, 95\% CI = 1.4-482.7) was found to be an independent predictor of oxidative stress in patients with AA. Increased severity of AA was found as an independent risk factor for IMA. Conclusion: Long-lasting disease, male sex, >1 site of involvement of disease, and increased severity of disease were correlated with increased oxidation. Presence of AA, male sex, and severe disease were determined to be independent risk factors for antioxidant and oxidant systems. IMA has great potential as a biomarker of oxidative stress in AA when compared to other studied biomarkers

Impaired enzymatic antioxidant defense mechanism in cancerous human thyroid tissues

The activities of total superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and catalase (CAT) enzymes were measured in cancerous and non-cancerous adjacent tissues from 15 patients with follicular thyroid cancer containing single nodule. SOD and GSH-Px activities were found lower but malondialdehyde levels higher in cancerous tissues compared with those of noncancerous ones. However, no difference was found between CAT activities of the tissues. Activity decrease of GSH-Px enzyme in cancerous tissue was greater than that of SOD enzyme. Results suggested that enzymatic free radical defense system was significantly impaired and lipid peroxidation increased in the cancerous human thyroid tissues

The protective effects of dexmedetomidine on hepatic ischemia reperfusion injury

PubMed: 25428535Objective: The aim of this study was to evaluate the effect of dexmedetomidine (100 ?g/kg-ip) on liver ischemia and reperfusion (I/R) in rats. Methods: Twenty-four Wistar Albino rats were separated into three groups as control (C), ischemia-reperfusion injury (I/R) and dexmedetomidine group (I/R-D). Ischemia was induced with portal clampage for 45 minutes and reperfusion period was 45 minutes after declampage. Group I/R-D was received dexmedetomidine 100 ?g/ kg i.p. 30 min before portal clampage. Thiobarbutiric Acid-Reactive Substances (TBARS), glutathioneS-transferase (GST), superoxide dismutase (SOD), Catalase (CAT), and Paraoxonase 1 (PON-1) were investigated in blood samples. Also HSP60 and p53-positive hepatocytes were counted under ImageJ image analysis program. Results: All parameters, except GST levels, were significant between the groups (p < 0.05). Although HSP60 expression was significantly increased between I/R, I/R-D and C groups there were no significant differences between I/R-D and C (p = 0.443). On the other hand, p53 expression was also significantly increased between I/R, I/R-D and C groups At the same time, there were no significant differences between I/R-D and C groups (p = 0.354). Conclusion: All the results suggest that dexmedetomidine has beneficial effects on liver ischemia/reperfusion stress

The efficacy of dexmedetomidine on lung injury induced by renal ischemia/reperfusion in diabetic rats

Objectives: Ischemia-reperfusion (IR) injury is a complex phenomenon, which is known to cause cell damage. In this study, we aimed to investigate the protective effects of dexmedetomidine on lung in the renal IR model in diabetic rat

Effect of dexmedetomidine on ischemia-reperfusion injury of liver and kidney tissues in experimental diabetes and hepatic ischemia-reperfusion injury induced rats

Arslan, Mustafa/0000-0003-4882-5063WOS: 000403851700006Background: Reperfusion following ischemia can lead to more injuries than ischemia itself especially in diabetic patients. The aim of this study was to evaluate the effect of dexmedetomidine on ischemia-reperfusion injury (IRI) in rats with have hepatic IRI and diabetes mellitus. Methodology: Twenty-eight Wistar Albino rats were randomised into four groups as control (C), diabetic (DC), diabetic with hepatic ischemia-reperfusion injury (DIR), and diabetic but administered dexmedetomidine followed by hepatic IRI (DIRD) groups. Hepatic tissue samples were evaluated histopathologically by semiquantitative methods. Malondialdehyde (MDA), superoxide dismutase (SOD), glutathion s-transpherase (GST), and catalase (CAT) enzyme levels were investigated in liver and kidney tissues as oxidative state parameters. Results: In Group DIR; hepatocyte degeneration, sinusoidal dilatation, pycnotic nucleus, and necrotic cells were found to be more in rat hepatic tissue; while mononuclear cell infiltration was higher in the parenchyme. MDA levels were significantly lower; but SOD levels were significantly higher in Group DIRD with regard to Group DIR. In the IRI induced diabetic rats' hepatic and nephrotic tissues MDA levels, showing oxidative injury, were found to be lower. SOD levels, showing early antioxidant activity, were higher. Conclusion: The enzymatic findings of our study together with the hepatic histopathology indicate that dexmedetomidine has a potential role to decrease IRI