Melatonin: a hepatoprotective agent against radioiodine toxicity in rats

Barlas, Afşar; Sadic, Murat; Atilgan, Hasan Ikbal; Bağ, Yusuf Murat; Onalan, Ali Kemal; Yumuşak, Nihat; Şeneş, Mehmet; Fidanci, Vildan; Pekcici, Mevlüt Recep; Korkmaz, Murat; Kısmet, Kemal; Koca, Gökhan

doi:10.4149/bll_2017_020

Cited by 12 publications

(7 citation statements)

References 22 publications

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“…Rats treated under hypoxic conditions were widely used to investigate hypoxia‐induced oxidative stress in the liver, and AOPP levels in hypoxia‐treated rats could be used to evaluate protein oxidation and inflammation . In 2017, Barlas et al found that liver tissue AOPP levels were elevated in rats with radioiodine toxicity; it was determined that melatonin treatment could significantly decrease the AOPP levels compared to the radioiodine group. Moreover, Souza et al demonstrated that Pseudomonas aeruginosa infection increased the liver levels of AOPPs in experimentally infected silver catfish.…”

Section: Data Sourcesmentioning

confidence: 99%

Advanced oxidation protein products play critical roles in liver diseases

Zhao

Zhang

Ouyang

et al. 2019

Eur J Clin Investigation

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There is a complex oxidant and antioxidant system that maintains the redox homoeostasis in the liver. While suffering from exogenous or endogenous risk factors, the balance between oxidants and antioxidants is disturbed and excessive reactive oxygen species are generated, resulting in oxidative stress. Oxidative stress is prevalent in various liver diseases and is thought to be involved in their pathophysiology. Advanced oxidation protein products are generated under conditions of oxidative damage and are newly described protein markers of oxidative stress. Previous studies have underscored the universal pathogenic roles of oxidation protein products in various diseases. However, investigations into how these products participate in the development of liver diseases have been superficial and insufficient. In this review, we highlight the current understanding of the roles of advanced oxidation protein products in liver disease pathogenesis and the underlying mechanisms. Moreover, we summarize the current studies on advanced oxidation protein products in infectious and noninfectious, acute and chronic liver diseases. Different strategies for targeting these advanced oxidation protein products and future perspectives, which may pave the way for developing new therapeutic strategies, will also be discussed here.

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Section: Data Sourcesmentioning

confidence: 99%

Advanced oxidation protein products play critical roles in liver diseases

Zhao

Zhang

Ouyang

et al. 2019

Eur J Clin Investigation

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“…A rat model treated with intraperitoneal dexmedetomidine for preventing RAI-induced early liver damage observed that the rats treated with dexmedetomidine had lower mean scores of histopathologic parameters and lower malondialdehyde levels and higher total sulfhydryl and catalase activities than the RAI group [9]. Similarly, intraperitoneal melatonin treatment decreased the tissue advanced the oxidation of protein products and malondialdehyde levels and increase the total sulfhydryl level as well as reducing the early histopathologic damage of the liver after RAIT [34]. Moreover, montelukast had a partial radioprotector effect against the long-term liver damage at the third month of RAIT, particularly in terms of hyperemia and capsule thickening [10].…”

Section: Discussionmentioning

confidence: 99%

Ameliorating effects of N-acetyl cysteine against early liver damage of radioiodine in rats

Kuşkonmaz¹,

Demirel

Koca

et al. 2021

Nuclear Medicine Communications

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Objective The present study was aimed to explore the potential ameliorating effects of N-acetyl cysteine (NAC) against radioiodine (RAI)-induced early liver damage. Methods Thirty Wistar Albino male rats were arbitrarily allocated into three groups each containing 10 rats: the control group (group 1); the RAI group (group 2), oral 111 MBq/kg radioiodine was administered to rats; the RAI + NAC group (group 3), 150 mg/kg/day intraperitoneal NAC treatment was initiated 3 days prior to the RAI administration and continued for 10 days. Liver samples were obtained 24 h after the last dose of NAC therapy for biochemical and histopathologic evaluation. Results In the RAI + NAC group, the histopathologic damage was found significantly less than in the RAI group for whole parameters except inflammatory cell infiltration (P < 0.05). Unlike the RAI group which had marked histopathologic damage, the RAI + NAC group had only mild histologic activity index scores with no granuloma formation observed. Oxidative stress parameters were demonstrated that the NAC treatment significantly decreased the tissue malondialdehyde (MDA) and catalase levels and increased the total sulfhydryl (total sulfhydryl) levels when compared to the RAI group (P < 0.01). Conclusion The outcomes of the study exhibited that the NAC treatment improved RAI-induced early liver damage. This improving effect considered to be caused by its antioxidant, anti-inflammatory, and likely vasodilator properties of NAC. Having advantages such as inexpensive, easy access, and tolerability, the NAC can be used as a radioprotective agent, especially in patients with liver diseases and requiring RAI treatment.

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“…Therefore, there is a need for safe and effective protective agents to protect kidney during I 131 therapy and prevent secondary renal complications. Recent studies have reported positive results with antioxidant supplements for the prevention of RAIinduced extrathyroidal tissue damage (4,5,13,29).…”

Section: Introductionmentioning

confidence: 99%

Proliferative and apoptotic evaluations of renal preventive effects of coenzyme Q10 in radioiodine-131 induced renal damage

Yumuşak

Koca

Akbulut

et al. 2022

Ankara Üniversitesi Veteriner Fakültesi Dergisi

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The aim of this study was to investigated anti-proliferative and antiapoptotic effects of coenzyme Q10 (CoQ10) in the prevention of radioiodine-131 (RAI) (I 131 ) induced kidney damage. A total of Wistar albino rats were separated into equal three groups (n = 8/group): Group 1 (control): untreated group; Group 2 (RAI): mCi/kg RAI oral route; Group 3 (RAI+CoQ10): 3 mCi/kg RAI oral route and intraperitoneally 30 mg/kg/day CoQ10. CoeQ10 treatment was started two days before RAI administration and was continued five days once daily after RAI.Pathomorphological parameters of kidneys were measured using hematoxylin-eosin and Masson's trichrome staining. Immunohistochemically; proliferating cell nuclear antigen (PCNA), caspase 8, caspase 9 and terminal deoxynucleotidyl transferasemediated deoxyuridine triphosphate nick end labeling (TUNEL) were used to determine proliferation and apoptosis. With the exception of the control group, varying degrees of inflammation, degeneration, necrosis, and interstitial/perivascular fibrosis were detected in the kidneys of all rats. This histopathological damage was found to be significantly less in CoQ10 group versus RAI group (P<0.05). The all immunohistochemical examinations demonstrated that administration of CoQ10 had reduced proliferation and apoptosis (P<0.05). The results of kidney histopathology and immunohistochemistry demonstrated that administration of CoQ10 had reduced inflammation, proliferation, and apoptosis. These findings show CoQ10 can play an important role in the radioprotection of kidneys against RAI-induced damage.

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Melatonin: a hepatoprotective agent against radioiodine toxicity in rats

Abstract: The results of this study demonstrated that melatonin reduced the harmful effects of RAI treatment on the liver. Anti-inflammatory and antioxidant activities are likely to be involved in the mechanism underlying the radio-protective effects of melatonin (Tab. 3, Fig. 1, Ref. 30).

Cited by 12 publications

References 22 publications

Advanced oxidation protein products play critical roles in liver diseases

Advanced oxidation protein products play critical roles in liver diseases

Ameliorating effects of N-acetyl cysteine against early liver damage of radioiodine in rats

Proliferative and apoptotic evaluations of renal preventive effects of coenzyme Q10 in radioiodine-131 induced renal damage

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