Anti-tyrosinase, anti-elastase, and antioxidant activities of some symmetric bisthiocarbohydrazone compounds

Symmetric bisthiocarbohydrazone compounds (1, 2, 3) were obtained by the condensation of thiocarbohydrazide with carbonyl compounds such as isatin (a heterocyclic ketone) and two hydroxyl aldehydes (2-hydroxybenzaldehyde, 2-hydroxy-1-naphthaldehyde) respectively, according to the previously reported methods. These synthesized compounds were evaluated in terms of their anti-tyrosinase, anti-elastase and antioxidant potentials in vitro. All of the tested compounds exhibited anti-tyrosinase and anti-elastase activities. It was observed that the inhibition increased with the increase of bisthiocarbohydrazone concentrations. Compound 1 showed the highest anti-tyrosinase activity. The anti-tyrosinase activity is decreasing in the following order; 2<3<1. Compound 1 showed also the highest anti-elastase activity. The anti-elastase activity is decreasing as 3<2<1. As a result, the most effective compound in terms of anti-tyrosinase and anti-elastase activities is bisthiocarbohydrazone derived from isatin. Compounds 2 and 3 with the hydroxyl substitution showed antioxidant activity close to Trolox. These compounds were found to have significant reducing effects and to be effective scavengers of DPPH

Vanadyl sulfate administration protects the streptozotocin-induced oxidative damage to brain tissue in rats

Diabetes mellitus manifests itself in a wide variety of complications and the symptoms of the disease are multifactorial. The present study was carried out to investigate the effects of vanadyl sulfate on biochemical parameters, enzyme activities and brain lipid peroxidation, glutathione and nonenzymatic glycosylation of normal- and streptozotocin-diabetic rats. Streptozotocin (STZ) was administered as a single dose (65 mg/kg) to induce diabetes. A dose of 100 mg/kg vanadyl sulfate was orally administered daily to STZ-diabetic and normal rats, separately until the end of the experiment, at day 60. In STZ-diabetic group, blood glucose, serum sialic and uric acid levels, serum catalase (CAT) and lactate dehydrogenase (LDH) activities, brain lipid peroxidation (LPO) and nonenzymatic glycosylation (NEG) increased, while brain glutathione (GSH) level and body weight decreased. In the diabetic group given vanadyl sulfate, blood glucose, serum sialic and uric acid levels, serum CAT and LDH activities and brain LPO and NEG levels decreased, but brain GSH and body weight increased. The present study showed that vanadyl sulfate exerted antioxidant effects and consequently may prevent brain damage caused by streptozotocin-induced diabetes

Protective effect of vanadyl sulfate on skin injury in streptozotocin-induced diabetic rats

The aim of the present study was to investigate the effect of vanadyl sulfate supplementation on the skin tissues of diabetic and control rats. In this study, 6-6.5 months old male Swiss albino rats were used. The animals were randomly divided into the following four groups: group I, control (nondiabetic intact animals); group II, vanadyl sulfate control; group III, streptozotocin (STZ)-diabetic animals and group IV, STZ-diabetic animals given vanadyl sulfate. The animals were made diabetic by intraperitoneal injection of a single dose of 65mg/kg STZ in 0.01M citrate buffer (pH=4.5). From day 1 to day 60, 100mg/kg vanadyl sulfate was given daily by gavage technique to one of the control and diabetic groups. Body weights and blood glucose levels were estimated on experimental days 0, 1 and 60. On the 60th day, skin tissue samples were taken, glutathione (GSH), lipid peroxidation (LPO), nonenzymatic glycosylation (NEG) and protein levels, catalase (CAT), superoxide dismutase (SOD) and glutathione-S-transferase (GST) activities were determined. Blood glucose, skin LPO and NEG levels increased, but skin GSH levels and CAT, SOD and GST activities decreased in the STZ group. Treatment with vanadyl sulfate reversed these effects. The present study showed that vanadyl sulfate exerted antioxidant properties and may prevent skin damage caused by diabetes

Purification and some properties of rose (<i style="">Fructus cynosbati)</i> hips invertase

109-114Invertase was purified from rose (Fructus cynosbati) hips by ammonium sulfate fractionation and hydroxyapatite column chromatography. The enzyme was obtained with a yield of 4.25% and about 10.48-fold purification and had a specific activity of 8.59 U/mg protein. The molecular mass of invertase was estimated to be 66.51 kDa by PAGE and 34 kDa by SDS-PAGE, indicating that the native enzyme was a homodimer. The enzyme was a glycoprotein and contained 5.86% carbohydrate. The Km for sucrose was 14.55 mM and the optimum pH and temperature of the enzyme were 4.5 and 40°C, respectively. Sucrose was the most preferred substrate of the enzyme. The enzyme also hydrolyzed D(+) raffinose, D(+) trehalose and inulin (activity 39.88, 8.12 and 4.94%, respectively of that of sucrose), while D(+) lactose, cellobiose and D(+) maltose showed no effect on the enzyme. The substrate specificity was consistent with that for a β-fructofuranoside, which is the most popular type in the higher plants. The enzyme was completely inhibited by HgCl2, MnCl2, MnSO4, FeCl3, Pb(NO3)2, ammonium heptamolybdate, iodoacetamide and pyridoxine hydrochloride. It was also inhibited by Ba(NO3)2 (86.32%), NH4Cl (84.91%), MgCl2 (74.45%), urea (71.63%), I2 (69.64%), LiCl (64.99%), BaCl2 (50.30%), Mg(NO3)2 (49.90%), CrCl3 (31.90%) and CuSO4 (21.45%) and but was activated by Tris (73.99%) and methionine (12.47%)

Selenium content of milk and milk products of turkey. II

Selenium content of 1028 milk and milk products of Turkey are presented in this study. The selenium content of human milk (colostrum, transitional, and mature milk), various kinds of milk [cow, sheep, goat, buffalo, paper boxes (3%, 1.5%, 0.012% fat), bottled milk, condensed milk (10% fat), mineral added milk (1.6%), and banana, strawberry, and chocolate milk] and milk products (kefir, yogurt, Ayran, various cheese, coffee cream, ice cream, butter, margarine, milk powder, and fruit yogurt) in Turkey were determined by a spectrofluorometric method. The selenium levels of cow milks collected from 57 cities in Turkey were also determined. Selenium levels in cow milk varied with geographical location in Turkey and were found to be lowest for Van and highest for Aksaray. The results [milk (cow, sheep, goat, buffalo and human) and milks products] were compared with literature data from different countries

Antioxidant and antiacetylcholinesterase activities of chard (Beta vulgaris L. var. cicla)

Plants have been used for many years as a source of traditional medicine to treat various diseases and conditions. Many of these medicinal plants are also excellent sources for phytochemicals, many of which contain potent antioxidant and antiacetylcholinesterase activities. Chard (Beta vulgaris L var. cicla) is widely spread in Turkey and used as an antidiabetic in traditional medicine. In the present study, the antioxidant activity and acetylcholinesterase inhibitor capacity of chard were examined. In addition, proline level of chard was determined. The antioxidant activity of water extract of chard was evaluated using different antioxidant tests. The results were compared with natural and synthetic antioxidants. The results suggest that chard may provide a natural source of antioxidant and antiacetylcholinesterase activities and proline content. (C) 2010 Elsevier Ltd. All rights reserved

Purification and some properties of rose (Fructus cynosbati) hips invertase

lnvertase was purified from rose (Fructus cynosbati) hips by ammonium sulfate fractionation and hydroxyapatite column chromatography. The enzyme was obtained with a yield of 4.25% and about 10.48-fold purification and had a specific activity of 8.59 U/mg protein. The molecular mass of invertase was estimated to be 66.51 kDa by PAGE and 34 kDa by SDS-PAGE, indicating that the native enzyme was a homodimer. The enzyme was a glycoprotein and contained 5.86% carbohydrate. The K-m for sucrose was 14.55 mM and the optimum pH and temperature of the enzyme were 4.5 and 40 degrees C, respectively. Sucrose was the most preferred substrate of the enzyme. The enzyme also hydrolyzed D(+) raffinose, D(+) trehalose and inulin (activity 39.88, 8.12 and 4.94%, respectively of that of sucrose), while D(+) lactose, cellobiose and D(+) maltose showed no effect on the enzyme. The substrate specificity was consistent with that for a beta-fructofuranoside, which is the most popular type in the higher plants. The enzyme was completely inhibited by HgCl2, MnCl2, MnSO4, FeCl3, Pb(NO3)(2), ammonium heptamolybdate, iodoacetamide and pyridoxine hydrochloride. It was also inhibited by Ba(NO3)(2) (86.32%), NH4Cl (84.91%), MgCl2 (74.45%), urea (71.63%), l(2) (69.64%), LiCl (64.99%), BaCl2 (50.30%), Mg(NO3)(2) (49.90%), CrCl3 (31.90%) and CuSO4 (21.45%) and but was activated by Tris (73.99%) and methionine (12.47%)

Effects of Melissa officinalis L. extract on the skin tissues of hyperlipidemic rats

In this study, the effects of Melissa officinalis L. on hyperlipidemic rats were investigated biochemically. The animals were fed a lipogenic diet consisting of 2 % cholesterol, 20 % sunflower oil and 0.5 % cholic acid added to normal chow and were given 3 % ethanol for 42 d. The extract was given gavage technique to rats a dose of 2 g/kg everyday for 28 d, after 14 d, experimental animals done hyperlipidemia. In hyperlipidemic groups, a reduction of the skin glutathione level (GSH), skin superoxide dismutase (SOD) activity and serum catalase (CAT), paraoxonase (PON) activity and an increase in serum cholesterol, total lipid, triglycerides and uric acid, gamma-glutamyl transferase activity (GGT) and skin cholesterol, total lipid, lipid peroxidation (LPO), nonenzymatic glycosylation (NEG) and skin CAT, lactate dehydrogenase (LDH), glutathione peroxidase (GP,) and myeloperoxidase (MPO) activity were observed. Treatment with Melissa officinalis L. extract reversed these effects. Present results show that Melissa officinalis L. extract has a protective effect against skin tissue damage as result of hyperlipidemia, in addition to hypolipidemic effect