Effects of testosterone on orchiectomy-induced oxidative damage in the rat hippocampus

Meydan, Sedat; Kuş, İlter; Taş, Ufuk; Ögetürk, Murat; Sancakdar, Enver; Dabak, Durrin Ozlem; Zararsız, İsmail; Sarsılmaz, Mustafa

doi:10.1016/j.jchemneu.2010.07.006

Cited by 49 publications

(38 citation statements)

References 34 publications

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“…These observations provide evidence that testosterone deficiency contributes to the deterioration of antioxidant defense mechanisms in cardiomyocytes. In this respect, the results of our study are consistent with those reported by Barp et al (24) and Kłapcińska et al (25) in hearts and Meydan et al (23) in the hippocampal tissue. Data regarding the potential antioxidant role of exogenous testosterone in the heart are very scarce, and conflicting results have been observed in different tissues.…”

Section: Discussionsupporting

confidence: 93%

“…Antioxidant defenses, both enzymatic and non-enzymatic, protect the cell from ROS that can cause oxidative damage (22). The cellular antioxidant defense system consists of SOD, GSH-Px and other related enzymes (23). This dynamic system must be precisely regulated in order to protect cells from oxidative damage.…”

Section: Discussionmentioning

confidence: 99%

“…Androgens have been shown to effectively prevent the formation of lipid peroxidation (29). It has been reported that testosterone administration leads to a decrease in MDA levels in rat liver (30) and brain (23,31). In the study by Sreelatha Kumari et al, administration of testosterone in castrated rats partially reversed the increase in lipid peroxidation in the hearts (28).…”

Section: Discussionmentioning

confidence: 99%

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Testosterone suppresses oxidative stress via androgen receptor-independent pathway in murine cardiomyocytes

Xing¹

2011

Mol Med Report

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Abstract. Evidence supports that oxidative stress exerts significant effects on the pathogenesis of heart dysfunction. On the other hand, the presence of specific androgen receptor (AR) in mammalian cardiomyocytes implies that androgen plays a physiological role in cardiac function, myocardial injury and the regulation of the redox state in the heart. This study used the testicular feminized (Tfm) and castrated male mice to investigate the effects of testosterone deficiency, physiological testosterone therapy and AR on oxidative stress in cardiomyocytes. Tfm mice have a non-functional AR and reduced circulating testosterone levels. Male littermates and Tfm mice were separated into 5 experimental groups: non-castrated littermate controls, castrated littermates, sham-operated Tfm, testosterone-treated castrated littermates and testosteronetreated sham-operated Tfm mice. Cardiomyocytes that were isolated from the left ventricle were used for determination of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) enzyme activities, and malondialdehyde (MDA) levels. Additionally, mitochondrial DNA (mtDNA) deletion mutations were detected by nested PCR. The SOD and GSH-Px enzyme activities of cardiomyocytes were decreased, and the MDA levels and the proportion of mtDNA mutations were increased in castrated and sham-operated Tfm mice compared to control mice. However, an increase was observed in the activities of SOD and GSH-Px enzyme as well as a decrease in MDA levels and the proportion of mtDNA mutations in the mice that had received testosterone therapy. These changes were statistically similar in castrated and sham-operated Tfm mice after testosterone therapy. In conclusion, it is testosterone deficiency that induces oxidative stress in cardiomyocytes. Physiological testosterone therapy is able to suppress oxidative stress mediated via the AR-independent pathway.

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Section: Discussionsupporting

confidence: 93%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Testosterone suppresses oxidative stress via androgen receptor-independent pathway in murine cardiomyocytes

Xing¹

2011

Mol Med Report

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“…Several studies have shown that testosterone replacement exerted beneficial effects on brain function, including the prevention of neuronal cell death, the balancing of brain oxidative stress and antioxidant activity, improvement of synaptic plasticity and the involvement of cognitive formation in animal models (Janowsky 2006, Meydan et al 2010, Filova et al 2013. Interestingly, growing evidence demonstrated that testosterone deficiency is associated with obese insulinresistance in men (Haffner et al 1994, Stellato et al 2000, Grossmann et al 2008, Shi et al 2013).…”

Section: Introductionmentioning

confidence: 99%

Dipeptidyl peptidase 4 inhibitor improves brain insulin sensitivity, but fails to prevent cognitive impairment in orchiectomy obese rats

Pintana¹,

Pongkan²,

Pratchayasakul³

et al. 2015

Journal of Endocrinology

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It is unclear whether the dipeptidyl peptidase 4 (DPP4) inhibitor can counteract brain insulin resistance, brain mitochondrial dysfunction, impairment of hippocampal synaptic plasticity and cognitive decline in testosterone-deprived obese rats. We hypothesized that DPP4 inhibitor vildagliptin improves cognitive function in testosterone-deprived obese rats by restoring brain insulin sensitivity, brain mitochondrial function and hippocampal synaptic plasticity. Thirty male Wistar rats received either a sham-operated (S, nZ6) or bilateral orchiectomy (ORX, nZ24). ORX rats were divided into two groups and fed with either a normal diet (ND (NDO)) or a high-fat diet (HFO) for 12 weeks. Then, ORX rats in each dietary group were divided into two subgroups (nZ6/subgroup) to receive either a vehicle or vildagliptin (3 mg/kg per day, p.o.) for 4 weeks. After treatment, cognitive function, metabolic parameters, brain insulin sensitivity, hippocampal synaptic plasticity and brain mitochondrial function were determined in each rat. We found that HFO rats exhibited peripheral and brain insulin resistance, brain mitochondrial dysfunction, impaired hippocampal synaptic plasticity and cognitive decline. NDO rats did not develop peripheral and brain insulin resistance. However, impaired hippocampal synaptic plasticity and cognitive decline occurred. Vildagliptin significantly improved peripheral insulin sensitivity, restored brain insulin sensitivity and decreased brain mitochondrial reactive oxygen species production in HFO rats. However, vildagliptin did not restore hippocampal synaptic plasticity and cognitive function in both NDO and HFO rats. These findings suggest that vildagliptin could not counteract the impairment of hippocampal synaptic plasticity and cognitive decline in testosterone-deprived subjects, despite its effects on improved peripheral and brain insulin sensitivity as well as brain mitochondrial function.

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“…Most neurodegenerative diseases results in memory impairment. The hippocampus has been shown to play an important role in both long-term and short-term memory as well as spatial navigation [17]. This study was designed to investigate the protective effects of kolaviron on the hippocampus following METH-induced neuronal damage, as the need for the search for neuroprotective substances continues to be necessity in the bid to curtail the consequences of neurodegenerative disorders.…”

Section: Introductionmentioning

confidence: 99%

Neuroprotective Effects of Kolaviron, a Biflavonoid Complex of <i>Garcinia kola</i>, on Rats Hippocampus against Methamphetamine-Induced Neurotoxicity

Ijomone¹,

Nwoha²,

Olaibi³

et al. 2012

Macedonian Journal of Medical Sciences

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Aim: To investigate the protective effects of kolaviron on brain weight and behavioural performance and the histology of the hippocampus of adult Wistar rats following methamphetamine challenge. Materials and Methods:Twenty four adult Wistar rats weighing between 150-200 g, randomly assigned into four groups of six each (Groups A, B, C, D) were used for this research. Group A served as control, while groups B and C were given single dose methamphetamine (10 mg/kg) intraperitoneally after group C was pre-treated with kolaviron (200 mg/kg) for 7 days and group D received cornoil (vehicle for kolaviron) only.Results: High level of methamphetamine-induced stereotypic movement was observed, and the onset was delayed by kolaviron administration. Animals administered methamphetamine only, showed significantly poor behavioural performance on the water maze after treatment when compared to the other groups (P<0.05). Histological analysis revealed neuronal destruction of the pyramidal layer of the hippocampus following methamphetamine administration. Kolaviron to some extent prevented destruction of pyramidal cells of the hippocampus in pre-treated rats. Conclusion:The present findings show the neuro-destructive effects of methamphetamine on hippocampal neurons and its ability to negatively affect behaviour and that kolaviron could prevent such behavioural deficit and also afford some protection to the hippocampus.

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Effects of testosterone on orchiectomy-induced oxidative damage in the rat hippocampus

Cited by 49 publications

References 34 publications

Testosterone suppresses oxidative stress via androgen receptor-independent pathway in murine cardiomyocytes

Testosterone suppresses oxidative stress via androgen receptor-independent pathway in murine cardiomyocytes

Dipeptidyl peptidase 4 inhibitor improves brain insulin sensitivity, but fails to prevent cognitive impairment in orchiectomy obese rats

Neuroprotective Effects of Kolaviron, a Biflavonoid Complex of <i>Garcinia kola</i>, on Rats Hippocampus against Methamphetamine-Induced Neurotoxicity

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