Please use this identifier to cite or link to this item: http://localhost:80/xmlui/handle/123456789/16329
Title: Methylphenidate‐induced hepatotoxicity in rats and its reduction by buspirone
Authors: Nausheen Alam
Rahila Ikram
Keywords: Methylphenidate
SGPT
SGOT
buspirone
haloperidol
Issue Date: 2-May-2018
Publisher: Karachi: Faculty of Pharmacy & Pharmaceutical Sciences University of Karachi
Citation: Alam, N., & Ikram, R. (2018). Methylphenidate-induced hepatotoxicity in rats and its reduction by buspirone. Pakistan Journal of Pharmaceutical Sciences, 31(3), 741-745.
Abstract: Methylphenidate is commonly use for the treatment of attention deficit hyperactivity disorder (ADHD), but its long term use was found to produce hepatic necrosis in mice. Purpose of this study was to investigate that coadministration of buspirone (drug which attenuates methylphenidate induced sensitization) may attenuate methylphenidate-induced hepatotoxic effects and to determine the effect of challenge dose of haloperidol (D2 antagonist that blocks the effects of methylphenidate in case of intoxication) on SGPT and SGOT levels in methylphenidate treated rats. Estimation of SGPT and SGOT were performed using kit method. Prolong oral administration of methylphenidate at a dose of 2.0 mg/kg/day, buspirone at a dose of 10 mg/kg/day, their co-administration and challenge dose of haloperidol (1 mg/kg i.p.) in rats increased SGPT concentration and decreased SGOT concentration, effect is more pronounced in methylphenidate treated rats and potentiate with administration of haloperidol challenge dose. In conclusion our analysis showed that methylphenidate and challenge dose of haloperidol is associated with elevation of SGPT in rats, which is attenuate in co-administration of methylphenidate buspirone treated rats. To quantify the risk of methylphenidate-induced hepatic injury and role of buspirone to reduce the injury further pharmacoepidemiological investigations are required.
URI: http://142.54.178.187:9060/xmlui/handle/123456789/16329
ISSN: 1011-601X
Appears in Collections:Issue 03

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