Evaluation of total antioxidant status, total oxidant status and oxidative stress index in patients with alopecia areata.

OBJECTIVES: In this study, we aimed to evaluate total oxidative stress and total antioxidant capacity in serum samples from patients with Alopesia Areata (AA) in our laboratory conditions. METHODS: In this study, 46 subjects with AA (26 females, 20 males) and the control subjects of 36 (20 females, 16 males) age- and sex-matched healthy volunteers from our hospital staffs were enrolled (the mean age was 23.7 ± 11.0 years). Blood samples were obtained following an overnight fasting state, and were collected on ice at 4°C. The serum samples were separated from the cells by centrifugation at 3000 rpm for 15 min and were stored at -80°C and used for the analysis of the Total Antioxidant Status (TAS) and Total Oxidant Status (TOS). RESULTS: Total Antioxidant Status (TAS) and Total Oxidant Status (TOS), Oxidative Stress Index (OSI) (TOS/TAS) levels of AA patients were 1.4777 ± 0.1986; 9.7490 ± 6.0445; 0.6593 ± 0.4069 respectively. TAS; TOS; OSI (TOS/TAS) levels of controls were 1.4028 ± 0.1687; 9.4627 ± 4.2781; 0.6875 ± 0.3232 respectively. TAS, TOS and OSI levels showed no significant difference between the control and AA group (p > 0.05). CONCLUSION: Future studies about AA pathogenesis should be based not only on oxidant/antioxidant balance but also on several other factors. Because it was observed that the disease showed recurrence in different situations. Since the selection criteria of patients is affected from disease severity and environmental and genetical factors, multicentric studies with better sampled patient population and higher patient number is required.

Angiotensin II-induced MAPK phosphorylation mediated by Ras and/or phospholipase C-dependent phosphorylations but not by protein kinase C phosphorylation in cultured rat vascular smooth muscle cells.

Angiotensin II (Ang II) induces a rapid increase in mitogen-activated protein kinase (MAPK) activity through the Ang II type 1 receptor in cultured rat vascular smooth muscle cells (VSMCs). In the present study, we examined the effects of the phospholipase C (PLC) inhibitor U73122, the protein kinase C (PKC) inhibitor GF109203X, and the Ras inhibitor farnesylthiosalicylic acid (FTS) on Ang II-induced activation of p42/p44 MAPKs in cultured VSMCs. Phosphorylation was shown using the Western blot technique with specific phospho-antibodies against MAPK proteins. The PLC inhibitor U73122 abolished the Ang II-induced MAPK activity, while the PKC inhibitor GF109203X only decreased it. There was also an inhibition observed with the Ras inhibitor, FTS on Ang II-induced MAPK activity. These data suggest that Ang II-induced MAPK phosphorylation through the Ang II type 1 receptor could be mediated by Ras and/or PLC-dependent phosphorylations but not by PKC phosphorylation.