The relationship between the second to fourth digit ratio and acne vulgaris.

BACKGROUND: Although the pathophysiology of acne vulgaris (AV) is not clear, androgens are thought to play an important role in its development through either an increased level of circulating androgens or end-organ sensitivity. The ratio of the length of the second and fourth digit (2D : 4D) has been hypothesized to reflect prenatal androgen exposure and/or an individual's sensitivity to androgens, with a low 2D : 4D ratio suggesting high prenatal androgen exposure. Interestingly, the prenatal androgen peak time period coincides with both the development of the sebaceous gland and digits. OBJECTIVES: To determine the relationship between digit ratio and AV. METHODS: Vernier caliper was used to take digit measurements of both patients and controls. Acne severity was assessed by using the International Consensus Conference on Acne Classification System. RESULTS: Data of 251 patients with AV (67.7% female) and 120 healthy controls (72.5% female), aged 16-40 years, were analysed. The 2D : 4D ratios of female patients with AV were significantly lower than healthy females in both hands. However, there was no significant difference between male acne cases and controls. Acne severity was positively correlated with the left 2D : 4D ratios and mean 2D : 4D ratio, whereas the duration of acne was negatively correlated with the right 2D : 4D ratios in females. CONCLUSION: Our results support the anatomical evidence of in utero androgen exposure and/or an individual's sensitivity to androgens in patients with AV and suggest that the 2D : 4D ratio might be a predictor of acne development, duration, and severity grade, at least in female patients.

Oxidative stress in acne vulgaris.

BACKGROUND: Acne vulgaris is one of the common dermatological diseases and its pathogenesis is multifactorial. In this study, we aimed to determine the effects of oxidative stress in acne vulgaris. MATERIALS AND METHODS: The study involved 32 patients with acne vulgaris in the patient group and 34 healthy adults in the control group. The parameters of oxidative stress such as catalase (CAT), superoxide dismutase (SOD), xanthine oxidase (XO), nitric oxide (NO) and malondialdehyde (MDA) in the venous blood of patients were measured spectrophotometrically. The values were compared with those of the control group. RESULTS: The serum levels of MDA and XO activity in the patients with acne vulgaris were significantly higher than those of the controls. A significantly lower SOD and CAT activity was found in the patient group than in the control group. Although the patient group had higher serum levels of NO than the control group, the difference was not statistically significant. CONCLUSION: These results suggest that oxidative damage may play a role in the pathogenesis of acne; therefore, significant alterations may occur in the antioxidant defence system.

Vitamin E protects against acetone-induced oxidative stress in rat red blood cells.

Acetone may induce oxidative stress leading to disturbance of the biochemical and physiological functions of red blood cells (RBCs) thereby affecting membrane integrity. Vitamin E (vit E) is believed to function as an antioxidant in vivo protecting membranes from lipid peroxidation. The aim of the present study was the evaluation of possible protective effects of vit E treatment against acetone-induced oxidative stress in rat RBCs. Thirty healthy male Wistar albino rats, weighing 200-230 g and averaging 12 weeks old were randomly allotted into one of three experimental groups: Control (A), acetone-treated (B) and acetone + vit E-treated groups (C), each containing ten animals. Group A received only drinking water. Acetone, 5% (v/v), was given with drinking water to B and C groups. In addition, C group received vit E dose of 200 mg/kg/day i.m. The experiment continued for 10 days. At the end of the 10th day, the blood samples were obtained for biochemical and morphological investigation. Acetone treatment resulted in RBC membrane destruction and hemolysis, increased thiobarbituric acid reactive substance (TBARS) levels in plasma and RBC, and decreased RBC vit E levels. Vit E treatment decreased elevated TBARS levels in plasma and RBC and also increased reduced RBC vit E levels, and prevented RBC membrane destruction and hemolysis. In conclusion, vit E treatment appears to be beneficial in preventing acetone-induced oxidative RBC damage, and therefore, it can improve RBC rheology.

Caffeic acid phenethyl ester improves oxidative organ damage in rat model of thermal trauma.

Severe burn injuries cause functional impairment in distant internal organs. Although this mechanism is not clear, it is possible that free radical toxicity plays an important role. Research in animals and clinical studies have shown that there is a close relationship between a lipid peroxidative reaction and secondary pathological changes following thermal injury. It has been demonstrated that antioxidant treatment prevents oxidative tissue damage associated with thermal trauma. This study was designed to determine the possible protective effect of caffeic acid phenethyl ester (CAPE) treatment against oxidative damage in the kidney and lung induced by thermal injury. Rats were decapitated either 1, 3 or 7 days after burn injury. CAPE was administered intraperitoneally immediately after thermal injury. Kidney and lung tissues were taken for the determination of malondialdehyde (MDA) level, myeloperoxidase (MPO), catalase (CAT), superoxide dismutase (SOD) and xanthine oxidase (XO) activities. Severe skin thermal injury caused a significant decrease in SOD and CAT activities, as well as significant increases in MDA level, XO and MPO activities in tissues during the postburn period. Treatment of rats with CAPE (10 micromol/kg) significantly elevated the decreased SOD and CAT activities, while it decreased MDA levels and MPO as well as XO activity.