Effect of protein malnutrition on the neurobehavioural toxicity of styrene in young rats
β Scribed by Vinay K. Khanna; Raushan Husain; Prahlad K. Seth
- Publisher
- John Wiley and Sons
- Year
- 1994
- Tongue
- English
- Weight
- 541 KB
- Volume
- 14
- Category
- Article
- ISSN
- 0260-437X
No coin nor oath required. For personal study only.
β¦ Synopsis
Neurotoxic effects of styrene on certain biochemical and behavioural indices were studied in young rats kept deficient in protein during the weaning period. Young rats fed a low-protein diet showed a significant decrease in the level of dopamine and an increase in frontocortical [3Hlserotonin binding in comparison to the group of rats fed a normal protein diet. These rats also showed a significant increase in foot shock-induced aggressive behaviour, while no changes in amphetamine-induced locomotor activity, levels of norepinephrine and serotonin and binding of [3H]spiperone to striatal membrane were observed. On exposure to styrene, rats fed a normal protein diet showed a decrease in dopamine level and an increase in foot shock-induced aggressive behaviour only, with no significant change in other parameters, in comparison to the respective controls. It was, however, interesting to note that when rats fed a low-protein diet were exposed to styrene they showed a significant decrease in the levels of norepinephrine, dopamine and serotonin and an increase in the binding of [3H]spiperone and ['HIS-HT to striatal and frontocortical membranes, respectively. A significant increase in foot shock-induced aggressive behaviour and amphetamine-induced locomotor activity was also observed in this group of animals in comparison to those fed a low-protein diet. The biochemical and behavioural data indicate that protein deficiency makes young animals more vulnerable and it is an important predisposing factor in the neurobehavioural toxicity of styrene.
π SIMILAR VOLUMES
Effects of cysteine on the pharmacokinetics of oltipraz were investigated after iv (10 mg/kg) and oral (30 mg/kg) administration to male control, protein-calorie malnutrition (PCM), and PCM with oral cysteine supplementation (PCMC) rats. It was reported that oltipraz was mainly metabolized via hepat