Jan Surman. Universities in Imperial Austria, 1848–1918. A Social History of a Multilingual Space

This article review:  Jan Surman. Universities in Imperial Austria, 1848–1918. A Social History of a Multilingual Space. Indiana: Pur­due University Press, 2019, 458 pp

Comparative cytotoxicity study of nicotine and cotinine on MRC-5 cell line

Nicotine has several health hazards regarding carcinogenic potential. It also imparts increased risk for respiratory, cardiovascular, and gastrointestinal disorders. Several mechanisms have been proposed for the carcinogenic potential, including effects on cell proliferation, inducing oxidative stress, DNA mutation, or inhibition of apoptosis. The cotinine metabolite is generally thought to have effects similar to nicotine in some experimental systems. The purpose of this study was to assess the nicotine and cotinine cytotoxicity on MRC-5 lung fibroblasts. The pulmonary fibroblasts were treated with various concentrations of nicotine or cotinine (in the range 1 µM – 2 mM) for 24 or 48 h and analyzed for cell viability by MTT test. The results indicated that high nicotine concentrations (2 mM) induced marked cell death (about 50%) in MRC-5 cell line. Cotinine showed lower toxicity than nicotine on the MRC-5 cells. In contrast to nicotine treatment, cells treated with cotinine continued to proliferate after the 48h incubation period

Therapeutic Drug Monitoring and Methods of Quantitation for Carbamazepine

Carbamazepine is an early anticonvulsant still used today in the treatment of several forms of epilepsy. An active metabolite in the human body contributes to its pharmacological effect. Carbamazepine metabolism has high inter-individual variability, such that it is relatively difficult to establish a direct link between dose and concentration, or between concentration and pharmacological effect. Carbamazepine is thus a good candidate for therapeutic drug monitoring (TDM). Good UV specific absorbance and high plasmatic concentrations allow for the use of UV detection, which is often more accessible than other methods of detection. This paper presents several methods used for the detection of carbamazepine in plasma, methods that are capable of detecting drug and metabolites at adequate levels/ acceptance criteria. These methods have possible application not only in pharmacokinetic, bioequivalence, and permeability studies, but also in the therapeutic drug monitoring of carbamazepine

HPTLC assay of nicotine and cotinine in biological samples

This study presents the development of a simple high-performance thin layer chromatography (HPTLC) method for the determination of nicotine and its metabolite cotinine in human plasma and urine. The following mobile phases: methanol: ammonia (100:1.5, v:v), chloroform: acetone: ammonia (48.75: 48.75: 2.5, v:v:v), methanol: chloroform: ammonia (48.75: 48.75: 0.5, v:v:v) and glass plates precoated with silicagel 60 F254 (20x20) as a stationary phase were used. Densitometric scanning was performed at 263 nm. Two different extraction procedures have been applied: liquid-liquid extraction using dichloromethane at alkaline pH and solid-phase extraction using C18 cartridges. Preliminary tests in order to establish the system of solvents for development, as well as the range of linearity, were conducted. The best separation of nicotine and cotinine was obtained by using methanol: chloroform: ammonia (48.75: 48.75: 0.5, v:v:v) as the mobile phase. The liquid-liquid extraction technique led to better results than solid phase extraction. The regression curves were linear (with a corresponding correlation coefficient higher than 0.99) in the quantities range of 200 ng–1000 ng/spot for both nicotine and cotinine. The UV spectra confirm the identification of nicotine and cotinine both in the standards and in the extracts after liquid-liquid extraction. The proposed method can be applied for the simultaneous evaluation of nicotine and cotinine in biological samples at toxic/lethal levels. Thus, the method may be applicable in lethal nicotine intoxication cases in forensic toxicological analysis

Integrating Ecosystem Services in Historically Polluted Areas: Bioremediation Techniques for Soils Contaminated by Heavy Metals

Bioremediation of soils contaminated by heavy metals is based on the use of specially selected plants able to reduce the hazards of toxic metals. Depending on the mode of action on the heavy metals existing in the soil and the place where the action takes place, the following mechanisms for soil phytoremediation are distinguished: phytostabilization, phytoextraction, phytoimobilization, rhizofiltration, or evapotranspiration. These mechanisms are complex and include the plant ability to reduce the mobility and bioavailability of heavy metals and other pollutants, to extract large amounts of heavy metals from the soil or to evaporate water together with various pollutants already reached in the rhizosphere. Decontamination of polluted soils by using bioaccumulative plants is proposed as an environmental-friendly alternative to the traditional physicochemical methods, being a sustainable method with a great potential in the terms of environmental protection and cost management

Comparative cytotoxicity study of nicotine and cotinine on MRC-5 cell line

Nicotine has several health hazards regarding carcinogenic potential. It also imparts increased risk for respiratory, cardiovascular, and gastrointestinal disorders. Several mechanisms have been proposed for the carcinogenic potential, including effects on cell proliferation, inducing oxidative stress, DNA mutation, or inhibition of apoptosis. The cotinine metabolite is generally thought to have effects similar to nicotine in some experimental systems. The purpose of this study was to assess the nicotine and cotinine cytotoxicity on MRC-5 lung fibroblasts. The pulmonary fibroblasts were treated with various concentrations of nicotine or cotinine (in the range 1 µM – 2 mM) for 24 or 48 h and analyzed for cell viability by MTT test. The results indicated that high nicotine concentrations (2 mM) induced marked cell death (about 50%) in MRC-5 cell line. Cotinine showed lower toxicity than nicotine on the MRC-5 cells. In contrast to nicotine treatment, cells treated with cotinine continued to proliferate after the 48h incubation period