Oxidative stress parameters in serum and low density lipoproteins of Hashimoto's thyroiditis patients with subclinical and overt hypothyroidism.

BACKGROUND: Although prooxidant and antioxidant status were reported to be changed in clinical and experimental hypothyroidism, obtained results are conflicting. In addition, in subclinical hypothyroidism, scarced and controversial data are available about oxidative stress. Therefore, we aimed to investigate prooxidant-antioxidant status only in Hashimoto's thyroiditis (HT) patients with subclinical (sHT) and overt hypothyroidism (oHT). SUBJECTS AND METHODS: Thirty sHT and 18 oHT patients and 30 healthy control subjects were included in the study. Endogenous and prooxidant 2,2'-azobis-(2-amidinopropane) hydrochloride (AAPH)-induced malondialdehyde (MDA), diene conjugate (DC), protein carbonyl (PC) and nitrotyrosine (NT) levels as well as ferric reducing antioxidant power (FRAP) were determined in serum. In addition, endogenous DC and copper-induced MDA levels were measured in low density lipoprotein (LDL) fraction. RESULTS: Although there were no significant difference in serum endogenous MDA and DC levels, AAPH-induced MDA levels were significantly increased in sHT patients. All these parameters increased in oHT patients. Serum PC levels were detected to be increased in both sHT and oHT patients. Serum FRAP values did not alter in sHT patients, but they lowered in oHT patients. Endogenous DC and copper-induced MDA levels in LDL fraction did not change in sHT patients. However, these parameters were detected to be increased significantly in oHT patients as compared to controls and sHT patients. CONCLUSION: In conclusion, there were significant increases in oxidative stress parameters in serum and LDL-fraction in oHT patients. However, oxidative stress was detected to stimulate partly in serum, but not LDL fraction in sHT patients.

Association of the CC chemokine receptor 5 (CCR5) polymorphisms with preeclampsia in Turkish women.

AIM: Endothelial dysfunction and inflammation are involved in the pathogenesis of preeclampsia. The CC chemokine receptor 5 (CCR5) modulates inflammation secondary to endothelial dysfunction and related vascular disorders, by initiating chemotaxis. In this study, we examined the frequency of two polymorphisms, the CCR5D32 deletion and the CCR5-59029 A/G promoter point mutation in women with preeclampsia. METHODS: The CCR5 polymorphisms were genotyped in 74 preeclamptic and 128 controls who had been unaffected by preeclampsia in previous pregnancies. Genotyping was performed with the polymerase chain reaction and restriction fragment length polymorphism. Statistical evaluations were made using the chi-square test or Fisher's exact test when appropriate. RESULTS: The percentage of wild-type allele bearers (?/?plus ?/D32 genotypes) in the preeclamptic group was significantly higher than that of non-bearers (98.6 vs.91.4%, P = 0.03, by the Fisher's exact test). The number of the individuals with D32/D32 genotype was significantly high in the control group (P = 0.035). D32 allele revealed a 2.3-fold protective effect against the risk of preeclampsia.When the percentage of G allele bearers of CCR5 59029A/G polymorphism was compared between the groups, a significant increase was seen in preeclamptics (P = 0.002). CONCLUSION: CCR5 polymorphisms significantly influenced the susceptibility to preeclampsia in our study population consisted of Caucasians. The role of chemokines in this syndrome appears to be an important issue.