A histopathological and stereological study of the effects of acetylsalicylic acid on doxorubicin-induced hepatotoxicity in mice

被引:2
作者
Gokce, Ayse Basardi [1 ]
Eren, Banu [1 ]
Sagir, Dilek [2 ]
Yilmaz, Burcu Demirel [3 ]
机构
[1] Ondokuz Mayis Univ, Dept Biol, Fac Arts & Sci, Samsun, Turkey
[2] Sinop Univ, Fac Hlth Sci, Nursing Dept, TR-57000 Sinop, Turkey
[3] Ordu Univ, Akkus Vocat Sch, Akkus Ordu, Turkey
关键词
Acetylsalicylic acid; doxorubicin; histopathology; liver; mice; stereology; VENOUS THROMBOEMBOLISM; LIPID-PEROXIDATION; VITAMIN-E; ASPIRIN; ANTHRACYCLINES; MITOXANTRONE; EFFICIENCY; APOPTOSIS;
D O I
10.1080/10520295.2020.1788724
中图分类号
Q81 [生物工程学(生物技术)]; Q93 [微生物学];
学科分类号
071005 ; 0836 ; 090102 ; 100705 ;
摘要
Doxorubicin (Dox) is an anthracycline antibiotic with antineoplastic activity. Acetylsalicylic acid (Asa) is recommended for use as a prophylactic for thromboembolism during treatment of cancers. We investigated liver toxicity due to combined use of Dox and Asa in chemotherapy regimens. We used 140 Swiss albino mice divided into four main groups: control, Dox, Asa, and Dox + Asa. Each group was subdivided into seven subgroups based on time of sacrifice, i.e., 6, 12, 24, 48 h and 7, 14, 21 days. Quantitative and histopathological changes in liver were assessed by light microscopy and stereology. The portal triad area of the Dox and Dox + Asa groups was increased significantly compared to controls at 6 h, whereas in the Asa group, the means were similar to controls. Assessment of histopathology indicated an increased time-dependent degeneration and necrosis of liver tissues in mice in the Dox and Dox + Asa groups. The protective effects of Asa were not evident in Dox + Asa group. When Dox and Asa were administered together, degenerative changes were greater than for in the group that was given Dox alone. We found that Asa and Dox combined therapy increased tissue damage.
引用
收藏
页码:251 / 256
页数:6
相关论文
共 29 条
[11]   Comparison of the structural changes induced by doxorubicin and mitoxantrone in the heart, kidney and intestine and characterization of the Fe(III) mitoxantrone complex [J].
Herman, EH ;
Zhang, J ;
Hasinoff, BB ;
Clark, JR ;
Ferrans, VJ .
JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY, 1997, 29 (09) :2415-2430
[12]   Doxorubicin treatment in vivo activates caspase-12 mediated cardiac apoptosis in both male and female rats [J].
Jang, YM ;
Kendaiah, S ;
Drew, B ;
Phillips, T ;
Selman, C ;
Julian, D ;
Leeuwenburgh, C .
FEBS LETTERS, 2004, 577 (03) :483-490
[13]  
Jordan M. A., 2002, Current Medicinal Chemistry - Anti-Cancer Agents, V2, P1, DOI 10.2174/1568011023354290
[14]   Doxorubicin hepatotoxicity and hepatic free radical metabolism in rats - The effects of vitamin E and catechin [J].
Kalender, Y ;
Yel, M ;
Kalender, S .
TOXICOLOGY, 2005, 209 (01) :39-45
[15]   Comparison of pharmacokinetic and pharmacodynamic profiles of aspirin following oral gavage and diet dosing in rats [J].
Kapetanovic, Izet M. ;
Bauer, Kenneth S. ;
Tessier, Daniel M. ;
Lindeblad, Matthew O. ;
Zakharov, Alexander D. ;
Lubet, Ronald ;
Lyubimov, Alexander .
CHEMICO-BIOLOGICAL INTERACTIONS, 2009, 179 (2-3) :233-239
[16]   The protective effect of beta-1,3-D-glucan on taxol-induced hepatotoxicity: a histopathological and stereological study [J].
Karaduman, Dilek ;
Eren, Banu ;
Keles, Osman Nuri .
DRUG AND CHEMICAL TOXICOLOGY, 2010, 33 (01) :8-16
[17]  
Karim S., 2001, Indian Journal of Pharmacology, V33, P203
[18]  
LIU Y, 1992, J PHARMACOL EXP THER, V263, P651
[19]   HEPATOTOXICITY OF MITOXANTRONE AND DOXORUBICIN [J].
LLESUY, SF ;
ARNAIZ, SL .
TOXICOLOGY, 1990, 63 (02) :187-198
[20]   THE HYDROXYLATION OF THE SALICYLATE ANION BY A FENTON REACTION AND GAMMA-RADIOLYSIS - A CONSIDERATION OF THE RESPECTIVE MECHANISMS [J].
MASKOS, Z ;
RUSH, JD ;
KOPPENOL, WH .
FREE RADICAL BIOLOGY AND MEDICINE, 1990, 8 (02) :153-162