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Mitochondrial Complex I Inhibition Depletes Plasma Testosterone in the Rotenone Model of Parkinson’S Disease

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Mitochondrial Complex I Inhibition Depletes Plasma Testosterone in the Rotenone Model of Parkinson’S Disease Physiology & Behavior 83 (2004) 395–400 Mitochondrial complex I inhibition depletes plasma testosterone in the rotenone model of Parkinson’s disease M. Alam, W.J Schmidt* Zoological Institute, Department of Neuropharmacology, Morgenstelle 28E, University of Tuebingen, 72076 Tuebingen, Germany Received 5 April 2004; received in revised form 29 July 2004; accepted 11 August 2004 Abstract Age-related depletion of testosterone may increase the brain’s vulnerability to parkinsonian- or Alzheimer’s-like neurodegenerative disorders. In rats, rotenone, a mitochondrial complex I inhibitor, causes specific nigral dopaminergic neurodegeneration producing parkinsonian symptoms. In this study, rotenone was administered on a daily basis (2 mg/kg i.p.) to two groups of rats, over a period of 30 and 60 days, respectively. In order to contribute towards the validation of the rotenone rat model, the changing level of the peripheral sex steroid hormone, testosterone, which would also mimic those found in Parkinson’s disease (PD) patients, was evaluated. Parallel to this, prolactin, luteinizing hormone (LH), the nonsexual steroid thyroid-stimulating hormone, and the corticosterone hormone levels in the peripheral blood plasma were measured to show whether other hormones have also been affected by complex I inhibition. The rotenone treatment caused a decrease of testosterone level in the peripheral blood plasma. There were no differences in the thyroid hormone and prolactin but increases in leutinizing hormone and corticosterone were observed. Data from this study indicate that rotenone depleted the sex steroid hormone which is preferentially produced in the periphery, e.g., adrenal gland and testis. In conclusion, because a decrease in testosterone levels is also one of the comorbidities which are found in male PD patients, our results indicate that the rotenone model mimics PD symptoms not only on a neuronal and behavioral level, but also on the testosterone levels. D 2004 Elsevier Inc. All rights reserved. Keywords: Androgen; Testosterone; Corticosterone; Prolactin; Complex I; Dopamine 1. Introduction The involvement of mitochondrial inhibition in neuro- degeneration has received particular attention. Mitochon- NADH-ubiquinone oxidoreductase deficiency of mito- drial abnormalities have been identified in more common chondrial complex I can be present in a wide variety of sporadic neurological disorders, including Alzheimer’s biochemical and symptomatic phenotypes. Complex I is a disease (AD) and Parkinson’s disease (PD), and they huge multienzyme complex of 43 separately encoded gene also occur as part of normal aging [25]. The chronic products derived from both nuclear and mitochondrial exposure of rotenone induces dopaminergic neuronal genomes [19,29]. Rotenone inhibits mitochondrial complex degeneration and formation of alpha-synuclein-positive I (NADH: ubiquinone oxidoreductase), which is a proximal cytoplasmic inclusions in nigral neurons [5,36].PDisa component of the mitochondrial electron transport chain movement disorder and mostly it is related to the (ETC), and it produces the energy necessary for main- disturbance of the nigrostriatal dopaminegric system. In tenance of all neuronal or cell functions. most cases of PD, the mesolimbic dopaminergic system is also disturbed, which plays an important role as a modulator of the complex reward process that organizes * Corresponding author. Tel.: +49 7071 2974571; fax: +49 7071 motivated behaviors, such as drinking, feeding and sex, 295144. by the elevation of salient environmental stimuli. The E-mail address: [email protected] (W.J. Schmidt). mesolimbic dopaminergic system is known to play an 0031-9384/$ - see front matter D 2004 Elsevier Inc. All rights reserved. doi:10.1016/j.physbeh.2004.08.010 396 M. Alam, W.J. Schmidt / Physiology & Behavior 83 (2004) 395–400 important facilitory role in copulation [26]. But it is clear general and more prominent influence on the brain than that in PD, the tubero-infundibular dopaminergic neurons reproduction and sexuality. are spared [1]. Although it is well known that most pesticides have a There is substantial evidence indicating that steroid pronounced effect on sex steroids, most of them are hormones modify vulnerability to neuronal insults. Pro- however not complex I inhibitors. Therefore, the present longed elevation of corticosterone was shown to increase study explored whether a specific complex I inhibitor has the vulnerability of nerve cells to the neurodegenerative a specific effect on the male sex steroid and other processes in aging, cerebral ischemia and possibly other hormones. neurodegenerative diseases [35]. An increase in levels of glucocorticoids, like corticosterone, may exert many of their toxic effects via an interaction with dopamine (DA) 2. Experimental procedures and glutamate. It has been shown that this stress hormone also inhibits the uptake of DA [9]. Likewise, glucocorti- 2.1. Animals coids can block the uptake of glutamate [14] which can further exacerbate the neurotoxic effect through excitotox- Forty adult male Sprague–Dawley rats (Charles River, icity. Gonadal steroids, like testosterone in the male, play a Sulzfeld, Germany) aged 7 weeks were chosen for the role in the nervous system development. A decrease in experiment. At the beginning of the experiment, the rats circulating testosterone contributes to an age-related weighed 230–240 g. Animals were housed in cages under a increase in glial fibrillary acidic protein (GFAP) which 12:12-h light/dark cycle in a room maintained at a constant could render the brain more susceptible to neurodegenera- temperature of 22 8C and 50–60% humidity with food and tion during aging [8]. Low serum testosterone has been water available ad libitum. To minimize the stress for the associated with poor cognitive performance in elderly men rats during the injections, they were weighed and handled and AD [20,28]. A number of in vivo studies have shown for 5 to 10 min the day before the injection. that androgens can rescue specific populations of moto- All treatments used in this experiment adhere to the neurons from both ontogenic- and axotomy-induced death. international ethical standards and the German Animal- In in vitro studies, it has been shown that glucose-deprived Protection Law and have been approved by local animal hippocampal neurons are rescued by testosterone and care committee (Tierschutzkommission, Regierungspra¨si- testosterone itself also acts as an antioxidant via andro- dium Tu¨bingen, ZP 2/03). gen-receptor-mediated mechanism [2,15]. Like other steroid hormones, the cellular effects of 2.2. Chemicals testosterone can be broadly grouped into genomic and nongenomic categories. The neuroprotective role of testos- Rotenone was purchased from Sigma (St. Louis, MO) terone is mostly known through the genomic pathway via an and was dissolved in sterile natural oil [middle chain androgen-receptor-dependent manner. The polyglutamine triglycerides (MCT); Miglyol 812, clinical pharmacy, (CAG) polymorphism of androgen receptors has been University Tuebingen]. Luciferin–luciferase enzymes were associated with the risk of AD in men and with other brain obtained from Sigma and protein assay kit from Bio-Rad disorders [24]. In the neonatal period, the presence of (Richmond, CA, USA). circulating testosterone is essential for the development of the substantia nigra region which exerts proconvulsant 2.3. Treatment effects throughout the rat’s life, a unique feature of the male substantia nigra. The final maturation of the substantia Rotenone emulsified in natural oil at 2.0 mg/ml was nigra occurs in the prepubertal period, and is, in part, given intraperitoneally once a day at 1 ml/kg during 60 regulated by testosterone as well [38]. The influence of days. Oil was injected as vehicle to control rats (1 ml/kg). testosterone in neurodegenerative diseases, such as PD and For the determination of the serum hormone assay and AD, can be translated into new cures of the disorders with tissue adenosine triphosphate (ATP) from the adrenal gland distinct sex-specific and more effective therapies. The level and testis, two groups of rats were used, namely, vehicle- of circulating testosterone plays a key role in the develop- treated (n=10) and rotenone-treated (n=10) groups. Control ment organization of the substantia nigra pars reticulata and groups received oil for 30 and 60 days and rats were treated its GABAA-ergic circuit that modify motor behavior in a with rotenone for 30 and 60 days. precise, age-dependent fashion [38]. In contrast, gonad steroids increase the number and size of tyrosine hydrox- 2.4. Blood sampling ylase (TH) immunoreactive neurons in some dopaminergic neurons’ population in both male and female rats [34,40]. Rats were killed by decapitation with the use of a Therefore, it seems that androgen levels are capable of guillotine after 30 and 60 days and the trunk blood was influencing dopaminergic function via modulation of TH collected after an overnight fast from both groups in a blood mRNA expression. The sex hormone testosterone has a sample tube containing lithium-heparin (15 IU heparin/ml). M. Alam, W.J. Schmidt / Physiology & Behavior 83 (2004) 395–400 397 2 vol (g/ml)], homogenized at 250–260 rpm for 3 min in the ice bath, and centrifuged at 960Âg at 4 8C for 15 min and followed by recentrifuging at 8000Âg for 10 min at 4 8C to give a supernatant. The supernatant was used to measure activities of ATP. 2.6. Hormone and tissue protein assay The in vitro testosterone test was carried out by enzyme sandwich immunoassay (Vitro ECI, Ortho Diagnostics, Rochester, NY, USA) in immunodiagnostics system. Intra- and interassay variations were b9.4%. The tissue protein assay was carried out using a Bio-Rad protein assay kit. 2.7. Evaluation of ATP content Tissue supernatants were incubated with a luciferin– luciferase mixture and the resulting luminescence was measured with a luminometer (LUMAT LB 9507; Berthhold Technologies, Bad Wildbad, Germany) according to the method [39] and the ratio ATP per unit protein was calculated. The analysis was done twice per animal. The mean values of relative intensityFS.D. was taken to plot the graph.
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