Effects of prolonged stanozolol treatment on antioxidant enzyme activities, oxidative stress markers, and heat shock protein HSP72 levels in rat liver

Pey, Ángel L.; Saborido, Ana; Blázquez, Isabel; Delgado, Jerónimo; Megías, Alicia

doi:10.1016/j.jsbmb.2003.09.001

Cited by 65 publications

(77 citation statements)

References 39 publications

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“…The increase in GPx activities in the liver as observed in the present study might be in response to H 2 O 2 produced by SOD activity since GPx play a significant role in the elimination of hydrogen peroxide [22]. Our results were in accordance with the previous reports by Camiletti-Moirón et al and Pey et al where brain and hepatic SOD and GPx activities were elevated in rat after chronic exposure to AAS [7,8]. GR activity significantly increased in the Su -treated groups.…”

Section: Alt (Iu/l) Ast (Iu/l) Alp (Iu/l)supporting

confidence: 94%

“…GPx, GR, while resistance training (RT) had no effect on antioxidants levels in male rat with and without training experience. This significant increase in hepatic antioxidants activity in the Su -treated groups is in harmony with Pey et al who observed that abuse of AAS for 8 weeks, either with or without concurrent exercise training, causes an increase the activities of the antioxidant enzymes in hepatic tissue as compared with control group [7]. On the contrary, Frankenfeld et al reported that the abuse of AAS decreases the liver antioxidants activity [20].…”

Section: Alt (Iu/l) Ast (Iu/l) Alp (Iu/l)supporting

confidence: 80%

“…The elevation of SOD, GPx and GR levels may be attributed to hepatic dysfunction of mitochondrial respiratory chain complexes and mono-oxygenase systems in response to Su administration [7,21], it would be possible that these alterations were accompanied by an increased ROS production. Excessive ROS formation could lead to oxidative stress and cell damage [22].…”

Section: Alt (Iu/l) Ast (Iu/l) Alp (Iu/l)mentioning

confidence: 99%

“…Available data have shown that AAS abusing is accompanied by increased of oxidative stress condition in the liver, brain, and heart [7][8][9][10].…”

Section: Introductionmentioning

confidence: 99%

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Effects of Resistance Training Accompanied by Sustanon Abuse on Hepatotoxicity in Rats with and without Training Experience

Rahmati¹,

Arazi²,

Ghafoori³

2017

Sports Nutr Ther

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Objectives: Abuse of anabolic androgenic steroids (AAS) has increased. Previous studies have shown that resistance training (RT) is the main exercise modality practiced by AAS abusers and people often use them in different training situations. Thus propose of this study was to evaluate the hepatotoxic effects of sustanon (Su) as an example of anabolic androgenic steroids in male rats with and without RT experience.Methods: Rats were divided into seven groups: control; Su -untreated sedentary rats (non-Su/ Sed); Sutreated sedentary rats (Su/Sed); Su -untreated trained rats (non-Su/Tr); Su -treated trained rats (Su/Tr); Suuntreated experience trained rats (non-Su/XTr); Su -treated experience trained rats (Su/XTr). Su -treated groups received sustanon 10 mg/kg intramuscularly once a week for 8 weeks. In the Tr and XTr groups, the animals climbed a 1.1 m vertical ladder, 3 days per week for 8 and 12 week, respectively. Results:After Su -treatment, the mean values of serum parameters related to hepatic function were within normal ranges. Superoxide dismutase (SOD), glutathione peroxidase (GPx), and glutathione reductase (GR) activities were higher (P<0.05) in the liver of Su treatment groups. Tr and XTr did not change any of the above parameters. Conclusion:The present findings suggest that the injection of Su during 8 weeks, either with or without RT up-regulation of enzymatic antioxidant activities. Moreover, these data demonstrated that liver function tests do not always reflect liver abnormalities particularly at the initial stages.

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Section: Alt (Iu/l) Ast (Iu/l) Alp (Iu/l)supporting

confidence: 94%

Section: Alt (Iu/l) Ast (Iu/l) Alp (Iu/l)supporting

confidence: 80%

Section: Alt (Iu/l) Ast (Iu/l) Alp (Iu/l)mentioning

confidence: 99%

“…Available data have shown that AAS abusing is accompanied by increased of oxidative stress condition in the liver, brain, and heart [7][8][9][10].…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Effects of Resistance Training Accompanied by Sustanon Abuse on Hepatotoxicity in Rats with and without Training Experience

Rahmati¹,

Arazi²,

Ghafoori³

2017

Sports Nutr Ther

View full text Add to dashboard Cite

show abstract

“…On the other side, some researchers believed that some toxicants can result in an enhanced production of reactive oxygen species (ROS) in cells/tissues and exert oxidative stress (OS), which, in turn, increases the rates of cellular damage [44]. Pey et al (2003) showed that prolonged stanozolol treatment as an AAS can cause an oxidative stress situation in rat liver [45]. Therefore, it seems logical that the physical/chemical-induced oxidative stress may affect the testicular antioxidant system and lipid peroxidation [46].…”

Section: Pathological Changes Of Testes Ultrastructurementioning

confidence: 99%

Transmission Electron Microscopy for the Quantitative Analysis of Testis Ultra Structure

Shokri¹,

Hemadi²,

Aitken³

2012

The Transmission Electron Microscope

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Reactive Oxygen Species in Pulmonary Vascular Remodeling

Aggarwal

Groß

Sharma

et al. 2013

Comprehensive Physiology

126

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The pathogenesis of pulmonary hypertension is a complex multifactorial process that involves the remodeling of pulmonary arteries. This remodeling process encompasses concentric medial thickening of small arterioles, neomuscularization of previously nonmuscular capillary-like vessels, and structural wall changes in larger pulmonary arteries. The pulmonary arterial muscularization is characterized by vascular smooth muscle cell (SMC) hyperplasia and hypertrophy. In addition, in uncontrolled pulmonary hypertension, the clonal expansion of apoptosis-resistant endothelial cells leads to the formation of plexiform lesions. Based upon a large number of studies in animal models, the three major stimuli that drive the vascular remodeling process are inflammation, shear stress and hypoxia. Although, the precise mechanisms by which these stimuli impair pulmonary vascular function and structure are unknown, reactive oxygen species (ROS)-mediated oxidative damage appears to play an important role. ROS are highly reactive due to their unpaired valence shell electron. Oxidative damage occurs when the production of ROS exceeds the quenching capacity of the anti-oxidant mechanisms of the cell. ROS can be produced from complexes in the cell membrane (nicotinamide adenine dinucleotide phosphate-oxidase), cellular organelles (peroxisomes and mitochondria), and in the cytoplasm (xanthine oxidase). Furthermore, low levels of tetrahydrobiopterin (BH4) and L-arginine the rate limiting co-factor and substrate for endothelial nitric oxide synthase (eNOS), can cause the uncoupling of eNOS, resulting in decreased NO production and increased ROS production. This review will focus on the ROS generation systems, scavenger antioxidants, and oxidative stress associated alterations in vascular remodeling in pulmonary hypertension.

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Effects of prolonged stanozolol treatment on antioxidant enzyme activities, oxidative stress markers, and heat shock protein HSP72 levels in rat liver

Cited by 65 publications

References 39 publications

Effects of Resistance Training Accompanied by Sustanon Abuse on Hepatotoxicity in Rats with and without Training Experience

Effects of Resistance Training Accompanied by Sustanon Abuse on Hepatotoxicity in Rats with and without Training Experience

Transmission Electron Microscopy for the Quantitative Analysis of Testis Ultra Structure

Reactive Oxygen Species in Pulmonary Vascular Remodeling

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