Instability Due to Drug-Induced Vestibulotoxicity

OBJECTIVE: The therapeutic use of ototoxic drugs is relatively common, particularly in patients with severe diseases. It is likely that disturbances of balance in these patients are underestimated by clinicians. MATERIALS and METHODS: The purpose of this study was to identify drugs involved in the vestibulotoxic origin of instability in a group of 18 patients. RESULTS: Six patients showed both cochlear and vestibular damage, while 12 were affected only by posterior labyrinthine damage. Four groups of drugs were identified: antibiotics (nine patients), cytostatics (four), anti-tuberculosis medicinal products (three), and other drugs (two). Cytostatics were involved in many cases studied, a fact scarcely reported before. CONCLUSION: It is important to ensure an early diagnosis to prevent ototoxic effects induced by drugs. We propose that patients receiving potential ototoxic drugs undergo cochlear and vestibular assessments. Further, we recommend that patients with instability undergo vestibular rehabilitation.S

Brain oxidative stress and selective behaviour os aluminium in specific areas of rat brain: potential effects in a 6-OHDA-indiced model of Parkinson's disease

This is the peer reviewed version of the following article: Sofía Sánchez-Iglesias, Estefanía Méndez-Álvarez, Javier Iglesias-González, Ana Muñoz-Patiño, Inés Sánchez-Sellero, José Luís Labandeira-García, Ramón Soto-Otero. Brain oxidative stress and selective behaviour of aluminium in specific areas of rat brain: potential effects in a 6-OHDA-induced model of Parkinson’s disease. J. Neurochem. (2009) 109, 879–888, which has been published in final form at https://doi.org/10.1111/j.1471-4159.2009.06019.x. This article may be used for non-commercial purposes in accordance with Wiley Terms and Conditions for Use of Self-Archived Versions. This article may not be enhanced, enriched or otherwise transformed into a derivative work, without express permission from Wiley or by statutory rights under applicable legislation. Copyright notices must not be removed, obscured or modified. The article must be linked to Wiley’s version of record on Wiley Online Library and any embedding, framing or otherwise making available the article or pages thereof by third parties from platforms, services and websites other than Wiley Online Library must be prohibited.The ability of aluminium to affect the oxidant status of specific areas of the brain (cerebellum, ventral midbrain, cortex, hippocampus, striatum) was investigated in rats intraperitoneally treated with aluminium chloride (10 mg Al3+/kg/day) for 10 days. The potential of aluminium to act as an etiological factor in Parkinson’s disease (PD) was assessed by studying its ability to increase oxidative stress in ventral midbrain and striatum and the striatal dopaminergic neurodegeneration induced by 6-hydroxydopamine in an experimental model of PD. The results showed that aluminium caused an increase in oxidative stress (TBARS, protein carbonyl content, and protein thiol content) for most of the brain regions studied, which was accompanied by a decrease in the activity of some antioxidant enzymes (superoxide dismutase, catalase, glutathione peroxidase). However, studies in vitro confirmed the inability of aluminium to affect the activity of those enzymes. The reported effects exhibited a regional-selective behaviour for all the cerebral structures studied. Aluminium also enhanced the ability of 6-hydroxydopamine to cause oxidative stress and neurodegeneration in the dopaminergic system, which confirms its potential as a risk factor in the development of PD.This study was supported by grants PGIDIT03PXIB20804PR (to R.S.-O.) and PGIDIT07CSA005208PR (to J.L.L.-G.) from XUGA (Santiago de Compostela, Spain), and grants SAF2007-66114 (to R.S.-O.) and BFU2006-07414 (to J.L.L.-G.) from Ministerio de Ciencia e Innovación (Madrid, Spain).S