2004Unpublished venueRequires access

Efficacy of Vitamin E treatment on haloperidol-induced tardive dyskinesia model rats

Tan Yun

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Abstract

Objective To investigate pathophysiological mechanism of tardive dyskinesia (TD) by treating the TD model rats with Vitamin E (Vit E). Methods Twenty-four male Sprague-Dawley (SD) rats were randomly assigned into the control, TD and TD + Vit E group, processed with saline, haloperidol + saline, haloperidol + Vit E respectively. Orofacial dyskinesia [Vacuous chewing movements (VCMs) and tongue protrusions] was evaluated at each weekend. Venous blood was collected at the end of 9-week research and the serum superoxide dismutase ( SOD) activity and malondialdehydescid ( MDA) were assayed. Results Haloperidol could cause orofacial dyskinesia in rats; Vit E might relieve these symptoms (decreased score:9. 1 ±8. 9) ,it was significant difference to compare with the TD rats (decreased score:0.6 ±4. 2;P 0. 05). Serum SOD activity [ (340±43) U/ml] was increased and MDA level [(20±6) nmol/ ml] was decreased significantly in the TD rats. These changes could be returned by Vit E treatment [SOD: (403±17) U/ml,MDA:(6±4) nmol/ml]. Conclusions Vit E can relieve orofacial dyskinesia of TD model rats effectively, oxidative damages might be the key factors of TD.

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Objective To investigate pathophysiological mechanism of tardive dyskinesia (TD) by treating the TD model rats with Vitamin E (Vit E). Methods Twenty-four male Sprague-Dawley (SD) rats were randomly assigned into the control, TD and TD + Vit E group, processed with saline, haloperidol + saline, haloperidol + Vit E respectively. Orofacial dyskinesia [Vacuous chewing movements (VCMs) and tongue protrusions] was evaluated at each weekend. Venous blood was collected at the end of 9-week research and the serum superoxide dismutase ( SOD) activity and malondialdehydescid ( MDA) were assayed. Results Haloperidol could cause orofacial dyskinesia in rats; Vit E might relieve these symptoms (decreased score:9. 1 ±8. 9) ,it was significant difference to compare with the TD rats (decreased score:0.6 ±4. 2;P 0. 05). Serum SOD activity [ (340±43) U/ml] was increased and MDA level [(20±6) nmol/ ml] was decreased significantly in the TD rats. These changes could be returned by Vit E treatment [SOD: (403±17) U/ml,MDA:(6±4) nmol/ml]. Conclusions Vit E can relieve orofacial dyskinesia of TD model rats effectively, oxidative damages might be the key factors of TD.

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Available abstract

Objective To investigate pathophysiological mechanism of tardive dyskinesia (TD) by treating the TD model rats with Vitamin E (Vit E). Methods Twenty-four male Sprague-Dawley (SD) rats were randomly assigned into the control, TD and TD + Vit E group, processed with saline, haloperidol + saline, haloperidol + Vit E respectively. Orofacial dyskinesia [Vacuous chewing movements (VCMs) and tongue protrusions] was evaluated at each weekend. Venous blood was collected at the end of 9-week research and the serum superoxide dismutase ( SOD) activity and malondialdehydescid ( MDA) were assayed. Results Haloperidol could cause orofacial dyskinesia in rats; Vit E might relieve these symptoms (decreased score:9. 1 ±8. 9) ,it was significant difference to compare with the TD rats (decreased score:0.6 ±4. 2;P 0. 05). Serum SOD activity [ (340±43) U/ml] was increased and MDA level [(20±6) nmol/ ml] was decreased significantly in the TD rats. These changes could be returned by Vit E treatment [SOD: (403±17) U/ml,MDA:(6±4) nmol/ml]. Conclusions Vit E can relieve orofacial dyskinesia of TD model rats effectively, oxidative damages might be the key factors of TD.

Key concepts: Tardive dyskinesia, Dyskinesia, Haloperidol, Superoxide dismutase, Saline, Pathophysiology, Medicine, Vitamin E

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