Uptake of radiodine by thyroid glan within 90 min after I.v injection with Na 131 I was studied in male rats which had been i.p injected with either PGB1, PGF1α or PGF2α. The mathematical analysis of radioiodide plasma disappearance curves showed that the rioiodide was kinetically exchanged within a two compartmental model. This is one of the three compartmental model of Wollman and Reed in which total 131 I is considered to be one compartment and blood plasma is the other. The fraction rate constant for migration of 131I from plasma pool towards the reversible pool of the thyroid was effectively enhanced by PGF1α and PGF2α . The reversible fractional rate constant was variably affected. The fractional rate constant that regulates the interconversion of free iodide from labile pool to be oxidized is increased due to the action of PGF1α and decreased by PGF2α.

Uptake of radiodine by thyroid glan within 90 min after I.v injection with Na 131 I was studied in male rats which had been i.p injected with either PGB1, PGF1α or PGF2α. The mathematical analysis of radioiodide plasma disappearance curves showed that the rioiodide was kinetically exchanged within a two compartmental model. This is one of the three compartmental model of Wollman and Reed in which total 131 I is considered to be one compartment and blood plasma is the other. The fraction rate constant for migration of 131I from plasma pool towards the reversible pool of the thyroid was effectively enhanced by PGF1α and PGF2α . The reversible fractional rate constant was variably affected. The fractional rate constant that regulates the interconversion of free iodide from labile pool to be oxidized is increased due to the action of PGF1α and decreased by PGF2α.

Uptake of radiodine by thyroid glan within 90 min after I.v injection with Na 131 I was studied in male rats which had been i.p injected with either PGB1, PGF1α or PGF2α. The mathematical analysis of radioiodide plasma disappearance curves showed that the rioiodide was kinetically exchanged within a two compartmental model. This is one of the three compartmental model of Wollman and Reed in which total 131 I is considered to be one compartment and blood plasma is the other. The fraction rate constant for migration of 131I from plasma pool towards the reversible pool of the thyroid was effectively enhanced by PGF1α and PGF2α . The reversible fractional rate constant was variably affected. The fractional rate constant that regulates the interconversion of free iodide from labile pool to be oxidized is increased due to the action of PGF1α and decreased by PGF2α.

Released T4 and T3 hormones in albino rat blood after an exogenous administration of PGB1, PG1α and PGF2α were determined and correlated with the serum content of calcium. Results revealed that all the tested PGs significantly raised the levels of T3 and T4 in rat serum, but not affect the serum calcium levels. PGB1 and PGF1α reduced the thyroidal calcium content due to enhancing the ellular permeability. However, the effect of PGF2α due to enhancing the lysosomal proteolytic enzyme activity.

Released T4 and T3 hormones in albino rat blood after an exogenous administration of PGB1, PG1α and PGF2α were determined and correlated with the serum content of calcium. Results revealed that all the tested PGs significantly raised the levels of T3 and T4 in rat serum, but not affect the serum calcium levels. PGB1 and PGF1α reduced the thyroidal calcium content due to enhancing the ellular permeability. However, the effect of PGF2α due to enhancing the lysosomal proteolytic enzyme activity.

Released T4 and T3 hormones in albino rat blood after an exogenous administration of PGB1, PG1α and PGF2α were determined and correlated with the serum content of calcium. Results revealed that all the tested PGs significantly raised the levels of T3 and T4 in rat serum, but not affect the serum calcium levels. PGB1 and PGF1α reduced the thyroidal calcium content due to enhancing the ellular permeability. However, the effect of PGF2α due to enhancing the lysosomal proteolytic enzyme activity.

Oxidative stress induced hyperglycemia plays a central role in the pathogenesis of diabetes and its complications in most of the tissues. In the present study the protective roles of lipoic acid and n-acetylcysteine for the treatment of oxidative stress in alloxan-induced diabetic rabbits were studied. The obtained results concluded that lipoic acid or N-acetylcystiene my be hseful for the therapy of oxidative stress associated with hyperglycemia. The beneficial action seems to result mainly from direct scavenging of ROS and restoring glutathione redox state.

Oxidative stress induced hyperglycemia plays a central role in the pathogenesis of diabetes and its complications in most of the tissues. In the present study the protective roles of lipoic acid and n-acetylcysteine for the treatment of oxidative stress in alloxan-induced diabetic rabbits were studied. The obtained results concluded that lipoic acid or N-acetylcystiene my be hseful for the therapy of oxidative stress associated with hyperglycemia. The beneficial action seems to result mainly from direct scavenging of ROS and restoring glutathione redox state.

Oxidative stress induced hyperglycemia plays a central role in the pathogenesis of diabetes and its complications in most of the tissues. In the present study the protective roles of lipoic acid and n-acetylcysteine for the treatment of oxidative stress in alloxan-induced diabetic rabbits were studied. The obtained results concluded that lipoic acid or N-acetylcystiene my be hseful for the therapy of oxidative stress associated with hyperglycemia. The beneficial action seems to result mainly from direct scavenging of ROS and restoring glutathione redox state.

Oxidative stress induced hyperglycemia plays a central role in the pathogenesis of diabetes and its complications in most of the tissues. In the present study the protective roles of lipoic acid and n-acetylcysteine for the treatment of oxidative stress in alloxan-induced diabetic rabbits were studied. The obtained results concluded that lipoic acid or N-acetylcystiene my be hseful for the therapy of oxidative stress associated with hyperglycemia. The beneficial action seems to result mainly from direct scavenging of ROS and restoring glutathione redox state.