PMID- 29477345
OWN - NLM
STAT- MEDLINE
DCOM- 20181114
LR  - 20181114
IS  - 1878-5867 (Electronic)
IS  - 0039-128X (Linking)
VI  - 134
DP  - 2018 Jun
TI  - Effects of stanozolol on apoptosis mechanisms and oxidative stress in rat cardiac 
      tissue.
PG  - 96-100
LID - S0039-128X(18)30032-1 [pii]
LID - 10.1016/j.steroids.2018.02.004 [doi]
AB  - Stanozolol is a widely used 17alpha-alkylated anabolic androgenic steroid (AAS) 
      derivative. Despite stanozolol's adverse effects, its effect on oxidative stress 
      parameters and mitochondrial apoptosis pathway is not clearly defined. In our 
      study, thirty four male Sprague-Dawley rats were divided into 5 groups as control 
      (C), vehicle control (VC), steroid (ST), vehicle control-exercise (VCE), and 
      steroid-exercise (STE). Animals were subcutaneously administered stanozolol 
      5 mg/kg in steroid groups and propylene glycol 1 ml/kg in the vehicle-control 
      groups. On the 28th day-after sacrification, oxidative stress (MDA, GSH, PC, SOD, 
      CAT) and apoptosis parameters (TUNEL, Cytochrome-c) in cardiac tissue were 
      evaluated. Also, blood vessel morphology of cardiac tissue was evaluated with 
      Verhoeff-van Giesen staining. It has been demonstrated that stanozolol 
      administration triggers apoptosis by using TUNEL assay and cytochrome-c 
      immunohistochemical staining intensity, while this effect is significantly 
      reduced in the presence of exercise. In conclusion, the present study 
      demonstrated that stanozolol administration induces apoptosis with increasing PC 
      and CAT levels, while GSH, MDA and SOD parameters do not reveal any significant 
      change. Exercise has a protective role in stanozolol induced oxidative stress and 
      apoptosis. According to Verhoeff-van Giesen staining results for blood vessel 
      morphology assessment, it has been seen that exercise has a protective role on 
      cardiac blood vessels. This mechanism needs further investigations with long term 
      exposure studies for clarifying possible pathways.
CI  - Copyright (c) 2018 Elsevier Inc. All rights reserved.
FAU - Kara, Mehtap
AU  - Kara M
AD  - Istanbul University, Faculty of Pharmacy, Department of Pharmaceutical 
      Toxicology, Istanbul, Turkey. Electronic address: mehtap.kara@istanbul.edu.tr.
FAU - Ozcagli, Eren
AU  - Ozcagli E
AD  - Istanbul University, Faculty of Pharmacy, Department of Pharmaceutical 
      Toxicology, Istanbul, Turkey.
FAU - Kotil, Tugba
AU  - Kotil T
AD  - Istanbul University, Istanbul Faculty of Medicine, Department of Histology and 
      Embryology, Istanbul, Turkey.
FAU - Alpertunga, Buket
AU  - Alpertunga B
AD  - Istanbul University, Faculty of Pharmacy, Department of Pharmaceutical 
      Toxicology, Istanbul, Turkey.
LA  - eng
PT  - Journal Article
DEP - 20180223
PL  - United States
TA  - Steroids
JT  - Steroids
JID - 0404536
RN  - 0 (Biomarkers)
RN  - 4R1VB9P8V3 (Stanozolol)
SB  - IM
MH  - Animals
MH  - Apoptosis/*drug effects
MH  - Biomarkers/metabolism
MH  - Blood Vessels/drug effects/metabolism
MH  - Male
MH  - Myocardium/*cytology/*metabolism
MH  - Oxidative Stress
MH  - Physical Conditioning, Animal
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Stanozolol/*pharmacology
OTO - NOTNLM
OT  - Apoptosis
OT  - Cardiac tissue
OT  - Immunohistochemistry
OT  - Oxidative stress
OT  - Stanozolol
EDAT- 2018/02/27 06:00
MHDA- 2018/11/15 06:00
CRDT- 2018/02/26 06:00
PHST- 2017/07/31 00:00 [received]
PHST- 2018/01/24 00:00 [revised]
PHST- 2018/02/15 00:00 [accepted]
PHST- 2018/02/27 06:00 [pubmed]
PHST- 2018/11/15 06:00 [medline]
PHST- 2018/02/26 06:00 [entrez]
AID - S0039-128X(18)30032-1 [pii]
AID - 10.1016/j.steroids.2018.02.004 [doi]
PST - ppublish
SO  - Steroids. 2018 Jun;134:96-100. doi: 10.1016/j.steroids.2018.02.004. Epub 2018 Feb 
      23.