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It is well known that bone markers (e.g. osteocalcin and alkaline phosphatase) play a significant role in healing of bone fractures, whereas oxidative stress delay such healing. The present study aimed to investigate the effect of a mixture of antioxidants (vitamins A, C, E, and selenium) on oxidative stress parameters, and the levels of bone healing markers in the plasma of male patients following fixative surgery of long bones. Antioxidant tablets (300 µg vitamin A, 10 mg vitamin E, 60 mg vitamin C, and 75 µg selenium) were administered to groups 3 and 4 (10 patients in each) for 1 and 2 weeks, respectively, in addition to the regular postoperative treatment. Groups 1 (25 patients) and 2 (10 patients) received the regular post-operative treatment consisting of intravenous (I.V.) second generation of cephalosporin 1000 mg/day for 3 days, oral diclofenac 50 mg, and paracetamol 500 mg twice daily for 15 days. Osteocalcin level and alkaline phosphatase activity as well as antioxidant enzymes superoxide dismutase (SOD), glutathione reductase (GR), as well as glutathione (GSH), and thiobarbituric acid reactive substances (TBARS) as indices of oxidative stress, were determined in the plasma of all patients after 1 or 2 weeks of long-bone fixative surgery. The results revealed that osteocalcin level and the activity of alkaline phosphatase were markedly increased in the plasma of patients who received antioxidants for 2 weeks. In addition, after 1 and/or 2 weeks, the levels of TBARS were significantly lower in the antioxidant-treated patients compared with those who did not receive antioxidants. On the other hand, the activities of SOD and GR were markedly elevated in plasma of patients who received antioxidants after 1 or 2 weeks compared with patients who received regular therapy. Moreover, the level of plasma GSH was markedly increased only after 2 weeks in patients who received antioxidants. It is concluded that administration of antioxidant vitamins A, E, and C in addition to selenium could accelerate bone healing after long-bone fixative surgery. Therefore, antioxidants should be considered in designing therapeutic protocols in post-operative bone surgery.

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Increased oxidative stress with high free radical generation has been described previously in animal models of hyperthyroidism. The present study was designed to investigate the protective effects of caffeic acid phenylethyl ester (CAPE) on oxidative damage in rats with experimentally induced hyperthyroidism. The study was conducted on 32 male Sprague-Dawley rats. The experimental animals were divided into four groups (control, CAPE alone, hyperthyroidism, and hyperthyroidism + CAPE). Hyperthyroidism was induced by intraperitoneal administration of 0.3 mg/kg/day  -thyroxine for 4 weeks. CAPE (10 µ g/kg) was administered intraperitoneally for 4 weeks. At the end of the experimental period, blood samples and various organs (liver, heart and brain) of rats were taken for the determination of thiobarbituric acid reactive substances (TBARS), reduced glutathione (GSH), oxidized glutathione, vitamin C and superoxide dismutase (SOD) levels and concentrations of triiodothyronine (T3), thyroxine (T4) and thyroxine-stimulating hormone (TSH). Our results indicate that TBARS, oxidized glutathione, SOD levels and concentrations of T3 and T4 were higher in plasma and tissues of the hyperthyroid group compared to controls. Vitamin C, GSH and TSH levels were decreased significantly in the hyperthyroid group when compared to the control group. CAPE treatment decreased the elevated TBARS, SOD, T3 and T4 levels and increased the lowered GSH, vitamin C and TSH levels to control levels in rats with hyperthyroidism. In conclusion, our results indicate that CAPE is beneficial as a protective agent against oxidative stress induced by hyperthyroidism in rats. The protection is probably due to multiple mechanisms involving free radical scavenger properties, attenuating lipid peroxidation and increasing the antioxidant status.The term hyperthyroidism is used for the overproduction of thyroid hormones from the thyroid gland and an excess of these hormones in the blood. Thyroid hormones accelerate the basal metabolic rate and oxidative metabolism by induction of specific mitochondrial enzymes [1], and hyperthyroidism accelerates reactive oxygen species (ROS) production and induces changes in the antioxidant protective systems of various tissues [2]. It is well documented that thyroid hormone administration to experimental animals induces oxidative stress in some tissues [3,4]. The cellular system is equipped with both enzymatic (superoxide dismutase, catalase, glutathione peroxidase and glutathione reductase) and non-enzymatic (glutathione and vitamins C, E and A) defences to counteract the ROS [5].In fact, enhancement in lipid peroxidation indicators occurs in liver, heart, muscle and testis [6,7] from hyperthyroid rats. In addition to lipid peroxidation, hyperthyroidism also promotes hepatic and heart protein oxidation [8,9]. These effects seem to be primarily determined through increased mitochondrial production of ROS [10] likely because of a greater mitochondrial content of the autoxidizable electron carriers [11]. Lipid pero...