Effects of propylthiouracil, propranolol, and vitamin E on lipid peroxidation and antioxidant status in hyperthyroid patients.

OBJECTIVE: The purpose of this study was to examine lipid peroxidation and antioxidant states during hyperthyroidism states and after given different treatments. DESIGN AND METHODS: We examined 44 hyperthyroid patients and 19 euthyroid healthy controls. Patients were divided into three groups according to the treatment: Propylthiouracil (PTU) group, PTU + propranolol (PRP) group, PTU + PRP + vitamin E (vitE) group. RESULTS: In the hyperthyroid patients plasma malondialdehyde (MDA) levels were significantly high as compared to the control group (p < 0,001). There was a significant decrease in the MDA levels post-treatment (p < 0.001 in the PTU + PRP group and PTU + PRP + vitE group, p < 0.01 in the PTU group). In the hyperthyroidism, blood reduced glutathione (GSH) levels were lower, erythrocyte superoxide dismutase (SOD) and catalase (CAT) activities were higher than in the control group, but these changes were not significant. Post-treatment in each of the three groups the GSH levels were increased significantly as compared to the pretreatment levels (p < 0.001). There was significant decrease in the SOD activity post treatment (p < 0.01 in all three groups). Post-treatment CAT activity was decreased (p < 0.05 in the PTU group, p < 0.001 in the other two groups). The erythrocyte glutathione peroxidase (Gpx) activity was lower significantly in the hyperthyroidism as compared to the control group (p < 0.001). Post-treatment, in the three groups Gpx activity increased significantly as compared to the pretreatment levels (p < 0.05 in the PTU group, p < 0.001 in the PTU + PRP group and PTU + PRP + vitE group). CONCLUSION: We considered that giving all three treatments would be useful to the prevention of oxidative stress in the hyperthyroidism states.

Effects of pentoxifylline and coenzyme Q10 in hepatic ischemia/reperfusion injury.

OBJECTIVES: We examined whether pentoxifylline (PTX) and coenzyme Q10 (Q) pretreatment affect ischemia-reperfusion damage in the rat liver. DESIGN AND METHODS: Twenty minutes of reflow following 30 min of ischemia was performed. Before the experiment, rats were treated PTX 50 mg/kg, IP or PTX 50 mg/kg IP + Q10 mg/kg, intragastric, or untreated. Rats were divided into four groups: control (C), ischemia-reperfusion (IR), PTX-treated (P), and Q+PTX-treated (QP) groups. Hepatic glutathione (GSH) and malondialdehyde (MDA) levels and catalase, superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and reductase (GSSGR) activities were measured. RESULTS: In IR group GSH levels decreased (p<0.01), conversely MDA levels increased (p<0.01). PTX pretreatment did not affect GSH and MDA values, but Q+PTX pretreatment improved of those (p<0.01). It was shown that catalase and GSH-Px activities increased during ischemia-reperfusion (p<0.01, both of), but PTX pretreatment did not significantly ameliorate those activities. GSSGR activity was higher in IR group than in basal levels (p<0.01). The decrease GSSGR activity that was observed in P group was not significant compared to IR group. During ischemia/reperfusion also SOD activity increased as compared with controls (p<0.05). In PTX-treated group, SOD activity was significantly higher than control and ischemia/reperfusion groups (p<0.01, both of). Q+PTX treatment ameliorated those enzyme activities to the control values. CONCLUSIONS: Short-term hepatic ischemia-reperfusion diminished GSH, increased MDA levels and induced some antioxidant enzyme activities. Q+PTX pretreatment was useful in hepatic ischemia-reperfusion injury, but treatment of PTX alone did not cause beneficial effect in the present study.

Pentoxifylline and N-acetylcysteine in hepatic ischemia/reperfusion injury.

This study was designed to clarify the effects of pentoxifylline (PTX) and N-acetylcysteine (NAC) on hepatic reperfusion injury in rats. Rats were pretreated with NAC, or PTX, or combination of the drugs. In each rat, liver was isolated after twenty minutes reperfusion following thirty minutes ischemia. Plasma alanine amino transferase (ALT) activity, liver tissue glutathione (GSH) and malondialdehyde (MDA) levels, glutathione peroxidase (GPx), glutathione reductase (GSSGR), superoxide dismutase (SOD) and catalase (CAT) activities were determined. Plasma ALT activity was higher in ischemia/reperfusion groups than in control. It was decreased in the groups given NAC. Administration of NAC maintained tissue GSH levels, whereas the levels were decreased in both the ischemia/reperfusion groups treated (P < 0.05) and untreated with PTX (P < 0.01). Increases in liver MDA concentration in ischemia/reperfusion (P < 0.01) and PTX-treated groups (P < 0.05) were mitigated by administration of NAC. GPx and CAT activities were increased in the ischemia/reperfusion (P < 0.01, P < 0.05) and PTX-treated groups (P < 0.05, P < 0.001). GSSGR activities were increased in the NAC (P < 0.001) and NAC-PTX-treated groups (P < 0.01). SOD activities were higher in the ischemia/reperfusion (P < 0.01) and the PTX-treated (P < 0.01) and the NAC-PTX-treated groups (P < 0.01 ). In conclusion, short-term liver ischemia/reperfusion diminished GSH, increased MDA and induced some antioxidant enzymes. While we could not find any useful effects with PTX as we expected, our findings indicate that NAC might be useful to prevent tissue damage in hepatic ischemia/reperfusion injury.