N-acetylcysteine supplementation reduces oxidative stress for cytosine arabinoside in rat model

被引：10

作者：

Balci, Yasemin Isik ^{[1
]}

Acer, Semra ^{[2
]}

Yagci, Ramazan ^{[2
]}

Kucukatay, Vural ^{[3
]}

Sarbay, Hakan ^{[1
]}

Bozkurt, Kerem ^{[2
]}

Polat, Aziz ^{[1
]}

机构：

[1] Pamukkale Univ, Dept Pediat Hematol & Oncol, Fac Med, Kinikli, Denizli, Turkey

[2] Pamukkale Univ, Dept Ophthalmol, Fac Med, Denizli, Turkey

[3] Pamukkale Univ, Dept Physiol, Fac Med, Denizli, Turkey

来源：

INTERNATIONAL OPHTHALMOLOGY | 2017年 / 37卷 / 01期

关键词：

Cytosine arabinoside; N-acetylcysteine; Keratoconjunctivitis; CANCER-CHEMOTHERAPY; DNA-DAMAGE; APOPTOSIS; CYTARABINE; PREVENTION; TOXICITY;

D O I：

10.1007/s10792-016-0259-7

中图分类号：

R77 [眼科学];

学科分类号：

100212 ;

摘要：

Cytosine arabinoside (ARA-C) is a pyrimidine analog that may cause keratoconjunctivitis when used in high doses. The underlying mechanism may be the increased amounts of reactive oxygen radicals that may damage the DNA synthesis of corneal and conjunctival epithelial cells. Topical corticosteroids are one of the prophylactic treatments for keratoconjunctivitis induced by ARA-C. Forty Wistar-type albino rats were included in this study the rats were divided into four groups. The first group (Group 1) received only ARA-C, the second group (Group 2) received ARA-C and N-acetylcysteine (NAC), the third group (Group 3) received only NAC and the fourth group (Group 4) was the control group. The total oxidant status (TOS), the total antioxidant capacity and the oxidative stress index (OSI) measurements of the cornea and the conjunctiva were evaluated in these four groups. The mean TOS and OSI value was the highest in Group 1 and the lowest in Group 3. The differences in TOS and OSI values were statistically significant between Group 1 and Group 2. There are decreases in TOS and OSI values in rats which received ARA-C with NAC administration. NAC may have a protective effect on ARA-C-induced keratoconjunctivitis.

引用

页码：209 / 214

页数：6

共 27 条

[1]

AlTweigeri T, 1996, CANCER, V78, P1359, DOI 10.1002/(SICI)1097-0142(19961001)78:7<1359::AID-CNCR1>3.0.CO

[2]

2-G

[3] N-Acetylcysteine prevents doxorubucine-induced cardiotoxicity in rats [J].

Arica, V. ;

Demir, I. H. ;

Tutanc, M. ;

Basarslan, F. ;

Arica, S. ;

Karcioglu, M. ;

Ozturk, H. ;

Nacar, A. .

HUMAN & EXPERIMENTAL TOXICOLOGY, 2013, 32 (06) :655-661

[4]

Cadet J, 1997, Rev Physiol Biochem Pharmacol, V131, P1

[5] Effects of n-acetylcysteine in a rat model of ischemia and reperfusion injury [J].

Cuzzocrea, S ;

Mazzon, E ;

Costantino, G ;

Serraino, I ;

De Sarro, A ;

Caputi, AP .

CARDIOVASCULAR RESEARCH, 2000, 47 (03) :537-548

[6] Mechanisms of N-acetylcysteine in the prevention of DNA damage and cancer, with special reference to smoking-related end-points [J].

De Flora, S ;

Izzotti, A ;

D'Agostini, F ;

Balansky, RM .

CARCINOGENESIS, 2001, 22 (07) :999-1013

[7] A novel automated method to measure total antioxidant response against potent free radical reactions [J].

Erel, O .

CLINICAL BIOCHEMISTRY, 2004, 37 (02) :112-119

[8] A new automated colorimetric method for measuring total oxidant status [J].

Erel, O .

CLINICAL BIOCHEMISTRY, 2005, 38 (12) :1103-1111

[9] Relevance of N-acetylcysteine in clinical practice:: Fact, myth or consequence? [J].

Faintuch, J ;

Aguilar, PB ;

Nadalin, W .

NUTRITION, 1999, 15 (02) :177-179

[10] Oxidative stress mediates neuronal DNA damage and apoptosis in response to cytosine arabinoside [J].

Geller, HM ;

Cheng, KY ;

Goldsmith, NK ;

Romero, AA ;

Zhang, AL ;

Morris, EJ ;

Grandison, L .

JOURNAL OF NEUROCHEMISTRY, 2001, 78 (02) :265-275

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