BackgroundA large number of essential oils is reported to have significant activity against Candida albicans. But the different chemical composition influences the degree of their activity. The intention of this study was to investigate the chemical composition and the activity against Candida albicans of volatile oils obtained from Artemisia dracunculus, A. abrotanum, A. absinthium and A. vulgaris (Asteraceae). The aim of the study was to identify new chemical compounds that have effect against C. albicans.The essential oils were obtained by hydrodistillation or extraction with dichloromethane (a new procedure we developed trying to obtain better, more separated compounds) from air dried above ground plant material and analyzed by GC-MS. Additionally commercial essential oils from the same species were tested. The Candida albicans inhibition studies were carried out by the paper disc diffusion method.ResultsThe essential oils shared common components but presented differences in composition and showed variable antifungal activity. Davanone and derivatives thereof, compounds with silphiperfolane skeleton, estragole, davanone oil, β-thujone, sabinyl acetate, herniarin, cis-chrysanthenyl acetate, 1,8-cineol, and terpineol were the main components of Artemisia volatiles.ConclusionsAmong the volatile fractions tested those from A. abrotanum containing davanone or silphiperfolane derivatives showed the highest antifungal activity. The in vitro tests revealed that the Artemisia oils are promising candidates for further research to develop novel anti-candida drugs.

Placental oxidative stress was suggested to play a role in the pathogenesis of pre-eclampsia (PE). In this study, levels of 8-hydroxy-2'-deoxyguanosine (8-OH-dG), a well-established marker of oxidative DNA damage, were analysed in placental cellular DNA from normal (group NP) and pre-eclamptic (group PE) pregnancies as well as from PE pregnancies complicated by intrauterine growth restriction (group PE-IUGR). Placental samples obtained immediately after delivery were frozen at -80 degrees C until analysis. Cellular DNA was isolated, hydrolysed and analysed using high-performance liquid chromatography. Native nucleosides were monitored at 254 nm and 8-OH-dG using electrochemical detection. Concentrations of 8-OH-dG were expressed as micro mol/mol 2'-deoxyguanosine. In group NP, mean concentration of 8-OH-dG reached 179.97+/-80.58 (+/-SEM; micro mol/mol dG). 8-OH-dG levels were higher in group PE (273.44+/-110.14 micro mol/mol), but the difference was not significant in comparison with group NP. Highest concentrations of 8-OH-dG were found in group PE-IUGR (428.97+/-141.40 micro mol/mol), with levels significantly higher than in group NP, but not group PE. The results indicate a positive correlation between the severity of PE and the degree of oxidative stress and corroborate previous studies suggesting reactive oxygen species to be involved in the pathophysiology of PE.

The study reveals this novel mucoadhesive delivery system to be a promising approach for buccal delivery of PACAP.

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In vehicles that are parked, no ventilation and/or air conditioning takes place. If a vehicle is exposed to direct solar radiation, an immediate temperature rise occurs. The high cabin air temperature can threaten children and animals that are left unattended in vehicles. In the USA, lethal heat strokes cause a mean death rate of 37 children per year. In addition, temperature-sensitive goods (e.g. drugs in ambulances and veterinary vehicles) can be adversely affected by high temperatures. To calculate the rise of the cabin air temperature, a dynamic model was developed that is driven by only three parameters, available at standard meteorological stations: air temperature, global radiation and wind velocity. The transition from the initial temperature to the constant equilibrium temperature depends strongly on the configuration of the vehicle, more specifically on insulation, window area and transmission of the glass, as well as on the meteorological conditions. The comparison of the model with empirical data showed good agreement. The model output can be applied to assess the heat load of children and animals as well as temperature-sensitive goods, which are transported and/or stored in a vehicle.

Aliphatic iV-nitrosomethylalkylamines exhibit a remarkable organ specificity in rats, the principal targets for tumour induction being liver, oesophagus, urinary bladder and lung. We have determined the extent of DNA methylation in these tissues following a single oral dose (0.1 mmol/kg; 6 h survival) of each of 12 homologues, ranging from N-nitrosodimethyiamlne (Cl) to A4utrosomethyldodecylamine (C12). Methylpurines (7-and O*-methylguanine) were determined by cation exchange HPLC with fluorescence detection. Highest levels of hepatic DNA methylation were found with A'-nkrosodimethjiainine (Cl) and A'-nitrosornethylethylamine (C2), the most potent bepatocarcinogens in this series. Concentrations of methylpurines in liver DNA decreased with increasing chain length for C1-C5. Administration of the higher homologues (C6-C12) caused levels of DNA methylation which by themselves were considered too low to account for their hepatocarcinogenicity. In rat oesophagus, DNA methylation closely paralleled carcinogenkity, the butyl and pentyl derivatives (C4, C5) being most effective. In rat lung, the extent of DNA methylation was generally lower and there was no apparent correlation with carcinogenicity. Methylation of kidney DNA also decreased with increasing chain length and was only detectable for C1-C5. In urinary bladder DNA, methylpurines were below or close to the limit of detection. It is concluded that the initiation of malignant transformation by DNA methylation alone (through hydroxylation at the methylene a-carbon) could be operative for Cl in kidney and lung, for Cl and C2 in liver, and C3-C5 in oesophagus. For the higher homologues, the extent of DNA methylation seems insufficient to explain the complex pattern of tissue specificity, suggesting that DNA modification other than, or in addition to, methylation may be responsible. IntroductionEarly investigations by Druckrey and co-workers (1) on the carcinogenicity of asymmetric nitrosamines in rats revealed a high degree of organ-specificity. Short-chain N-nitrosomethylalkylamines (Cl, C2*) induced predominantly rumours of liver and lung whereas the higher asymmetric homologues (C3-C6) produced exclusively or preferentially oesophageal neoplasms.

Polyclonal antibodies were developed in New Zealand White rabbits against DNA modified with diastereomeric benzo[c]phenanthrene-3,4-diol-1,2-epoxide (B[c]PhDE)-1 (4-hydroxyl and epoxide cis) and B[c]PhDE-2 (4-hydroxyl and epoxide trans). Antiserum developed against B[c]PhDE-2-DNA was stereoselective. In competitive ELISA assays using wells coated with 160 fmol B[c]PhDE-2-DNA adducts, B[c]PhDE-2-DNA gave 50% inhibition at 200 fmol adducts/well. B[c]PhDE-1-DNA required a 10-fold higher amount of adducts/well to give 50% inhibition. Benzo[a]pyrene-7,8-diol-9,10-epoxide-2-DNA and 7,12-dimethylbenz[a]anthracene-3,4-diol-1,2-epoxide-1-DNA caused only a 30% inhibition even at the highest doses tested (greater than 4000 fmol adducts/well). For antiserum developed against B[c]PhDE-1-DNA, 50% inhibition required 570 fmol B[c]PhDE-1-DNA adducts in wells coated with 100 fmol B[c]PhDE-1-DNA adducts. 7,12-Dimethylbenz[a]anthracene-3,4-diol-1,2-epoxide-1-DNA and B[c]PhDE-2-DNA were also effective competitors: they caused 50% inhibition at 1900 and 1800 fmol adducts/well respectively. In contrast, benzo[a]pyrene-7,8-diol-9,10-epoxide-2-DNA gave no inhibition at the highest dose of competitor tested (4050 fmol adducts/well). Antisera from three rabbits immunized with B[c]PhDE-2-DNA demonstrated similar antigen specificities. The properties of these antisera differ from those reported previously for antibodies developed against benzo[a]pyrene-DNA in that they show selectivity for DNA modified by specific hydrocarbon diolepoxides, in one case for B[c]PhDE-2-DNA and in the other for B[c]PhDE-DNA or 7,12-dimethylbenz[a]anthracene-3,4-diol-1,2-epoxide-1-DNA. The specificity of these antisera will facilitate analysis of the modification of DNA by different polycyclic aromatic hydrocarbon diolepoxides.