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River water in Kosovo is exposed to various discharges from industrial and agricultural activities as well as to urban wastewater. Rivers Sitnica and Drenica are among the most affected ones and water samples drawn from these rivers show the presence of various toxic substances. Genotoxic effects are seen in fish living in these rivers indicating a cytotoxic and mutagenic potential of the river water. Aiming at substantiating these observations, we assessed the cyto- and genotoxic effects of water samples collected at different locations from the Drenica and Sitnica rivers. Samples drawn from Lake Badovc served for comparison. To address seasonal effects, samples were collected at different seasons/time points during the period of summer 2016—spring 2018. The water samples were analyzed employing primary rat hepatocytes as a reliable in vitro cell model for the assessment of cytotoxic effects (mitotic arrest and cell death) and DNA damage/genotoxicity (micronucleus assay and Comet assay). The results do not account for significant effects associated with specific locations but demonstrate seasonal differences of the genotoxic potential of the water samples collected along both rivers, which are accompanied by a limited cytotoxic potential. Our data provide substantial support to earlier observations and strongly warrant the need for continuous chemical as well as biological monitoring of the river water in Kosovo, focusing on improved toxicant profiling of the river water and investigations addressing the observed seasonal variations. [ABSTRACT FROM AUTHOR]

The actual stage of the development of Kosovo is characterized by the concerning levels of environmental pollution and the serious health problems attributed to the emission of pollutants into air, soil and water. In this context, river pollution is one of the main threats due to the discharge of untreated urban and industrial waste waters that affect the quality of surface and ground water. In addition, urban and agricultural discharges are affecting the river water quality. In this article, we are presenting data on the cyto- and genotoxic potential of water samples from three rivers (Sitnica, Drenica and Lepenci) in the Kosovo as determined in the cultures of primary rat hepatocytes. Sitnica and Drenica (as the most important Sitnica tributary) drain into the Black Sea, whereas the Lepenci river drains into the Aegean Sea. These rivers are polluted mainly by industry in the Kosovo together with municipal discharges. The results of this study show that the samples have primarily a cytotoxic potential by causing necrotic cell death that was not accompanied by any increase of the rate of micronucleated cells as an indicator for a genotoxic potential. The different effects in 2 consecutive years can be attributed to variations in physico-chemical parameters such as water levels, intake of pollutants, and so on, indicating the need for continuous monitoring and risk assessment. [ABSTRACT FROM AUTHOR]

β-Carotene has been shown to increase the risk of developing lung cancer in smokers and asbestos workers in two large scale trails, the Beta-Carotene and Retinol Efficacy Trial (CARET) and the Alpha-Tocopherol Beta-carotene Cancer Prevention Trial (ATBC). Based on this observation, it was proposed that genotoxic oxidative breakdown products may cause this effect. In support of this assumption, increased levels of sister chromatid exchanges, micronuclei, and chromosomal aberrations were found in primary hepatocyte cultures treated with a mixture of cleavage products (CPs) and the major product apo-8' carotenal. However, because these findings cannot directly be transferred to the lung due to the exceptional biotransformation capacity of the liver, potential genotoxic and cytotoxic effects of β-carotene under oxidative stress and its CPs were investigated in primary pneumocyte type II cells. The results indicate that increased concentrations of β-carotene in the presence of the redox cycling quinone dimethoxynaphthoquinone (DMNQ) exhibit a cytotoxic potential, as evidenced by an increase of apoptotic cells and loss of cell density at concentrations > 10 µM. On the other hand, the analysis of micronucleated cells gave no clear picture due to the cytotoxicity related reduction of mitotic cells. Last, although CPs induced significant levels of DNA strand breaks even at concentrations ≥ 1 µM and 5 µM, respectively, -carotene in the presence of DMNQ did not cause DNA damage. Instead, β-carotene appeared to act as an antioxidant. These findings are in contrast with what was demonstrated for primary hepatocytes and may reflect different sensitivities to and different metabolism of β-carotene in the two cell types. [ABSTRACT FROM AUTHOR]

It has been reported by the Ministry of Environment in Kosova that particle emissions from one of the units of the coal-fired power plants (Kosova A) in Kastriot/Obiliq were exceeding the European standard by some 74 times. Besides the particle emission, there is also release of sulphur dioxide, mono-nitrogen oxide (NOx), carbon monoxide, carbon dioxide, organic compounds and heavy metals. In addition, there is also release of heavy metals and organic compounds from a nearby solid waste dumpsite. Together, they are considered to be responsible for the increased health problems of the population living in the vicinity.To study the genetic effects of these emissions we focused on the genetic load, that is, recessive mutations that affect the fitness of their carriers, of exposed wild living Drosophila melanogaster. The effects of ash from the dumpsite on the other hand were investigated upon feeding the ash with the nutrient medium. Our results revealed that the D. melanogaster population from the Kastriot/Obiliq area carries a high genetic load of 54.7%. Drosophila fed with the nutrient medium containing ash in a concentration of 1% carried a genetic load of 37.1%, whilst increasing concentrations (2% and 3% of ash) led to higher genetic loads of 68.7% and 67.4%, respectively. [ABSTRACT FROM AUTHOR]

This review on recent research advances of the lipid peroxidation product 4-hydroxy-nonenal (HNE) has four major topics: I. the formation of HNE in various organs and tissues, II. the diverse biochemical reactions with Michael adduct formation as the most prominent one, III. the endogenous targets of HNE, primarily peptides and proteins (here the mechanisms of covalent adduct formation are described and the (patho-) physiological consequences discussed), and IV. the metabolism of HNE leading to a great number of degradation products, some of which are excreted in urine and may serve as non-invasive biomarkers of oxidative stress. [ABSTRACT FROM AUTHOR]

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Iron and oxygen share a delicate partnership since both are indispensable for survival, but if the partnership becomes inadequate, this may rapidly terminate life. Virtually all cell components are directly or indirectly affected by cellular iron metabolism, which represents a complex, redox-based machinery that is controlled by, and essential to, metabolic requirements. Under conditions of increased oxidative stress-i.e., enhanced formation of reactive oxygen species (ROS)-however, this machinery may turn into a potential threat, the continued requirement for iron promoting adverse reactions such as the iron/H2O2-based formation of hydroxyl radicals, which exacerbate the initial pro-oxidant condition. This review will discuss the multifaceted homeodynamics of cellular iron management under normal conditions as well as in the context of oxidative stress. [ABSTRACT FROM AUTHOR]

Nigella sativa has attracted healers in ancient civilizations and researchers in recent times. Traditionally, it has been used in different forms to treat many diseases including asthma, hypertension, diabetes, inflammation, cough, bronchitis, headache, eczema, fever, dizziness and influenza. Experimentally, it has been demonstrated that N. sativa extracts and the main constituent of their volatile oil, thymoquinone, possess antioxidant, anti-inflammatory and hepatoprotective properties. In this review we aimed at summarizing the most recent investigations related to a few and most important effects of thymoquinone. It is concluded that thymoquinone has evidently proved its activity as hepatoprotective, anti-inflammatory, antioxidant, cytotoxic and anti-cancer chemical, with specific mechanisms of action, which provide support to consider this compound as an emerging drug. Further research is required to make thymoquinone a pharmaceutical preparation ready for clinical trials. [ABSTRACT FROM AUTHOR]

Optimal proliferation of cultured hepatocytes from normal rats occurs in response to epidermal growth factor (EGF) at an extracellular calcium concentration of 0.4 mM, whereas physiological concentrations of calcium have been shown to decrease hepatocyte proliferation. Exposure of hepatocytes to phenobarbital (PB, 0.1% in the drinking water) reduced significantly the ability of physiological levels of calcium to suppress hepatocyte proliferation. An increased relative ability of hepatocytes to proliferate at physiological calciumoncentrations versus that at 0.4 mM calcium was first seen after 3 days of PB treatment and this effect was maintained during 2 months of exposure. Hepatocytes from short-term PB-exposed animals (i.e. 3–28 days) proliferated at physiological Ca concentrations 2–3 times better than those from control animals. However, after 2 months of continuous PB exposure, cell growth was reduced significantly at all extracellular Ca concentrations investigated. EGF binding studies demonstrated thatthe biphasic kinetic effect of PB on hepatocyte proliferation was not correlated directly with the steady decline In EGF receptor number or the lack of significant change in receptor bindingaffinity with duration of PB exposure. These results imply that the effectiveness of PB in tumourpromotion may result from its ability to reduce the absolute magnitude of normal hepatocyte proliferation and to alter the growth regulatory effect of extracellular calcium. Further, the results argue that PB effects on hepatocyte proliferation are not mediated simply through regulation of EGF surface receptor number or binding affinity. Additional events of the EGF-induced cascade necessary for hepatocyte proliferation appear to be modified by PB. [ABSTRACT FROM PUBLISHER]

Primary cultures of adult rat hepatocytes were tested for their suitability to assess sister chromatid exchange (SCE)-inducing DNA damage produced by both directly and indirectly acting mutagens/carcinogens. Compared to other genotoxicity assay systems which utilize the metabolizing activity of liver microsomes, this system is at least 1–2 orders of magnitude more sensitive. The approximate drug concentrations leading to a doubling of control SCE levels were 2.5×10 M for cyclophosphamide, 4.5×10 M for dimethylnitrosamine, 2.5×10 M for -methyl--nitro--nitrosoguanidine, 2×10 M for aflatoxin B (AFB) and 30 mJ for u.v. The most potent inducer of SCE proved to be AFB, leading to a significantly elevated level of exchanges at a concentration of 10 M. The increased background SCE levels observed (0.75 SCE/chromosome) appears to reflect the sensitivity of hepatocytes to SCE-inducing DNA damage resulting from the dietary intake of mutagenic/carcinogenic compounds. In view of the high sensitivity and versatility of this genotoxicity assay system, it will be of use for the detection of the low levels of mutagenic/carcinogenic compounds found in the environment. [ABSTRACT FROM PUBLISHER]

Objectives: Utilizing primary rat hepatocytes we investigated the potential antimutagenic and anti-cytotoxic effects of carboxymethyl chitin-glucan (CM-CG) with respect to oxidative stress induced by the model free-radical-generating compounds hydrogen peroxide (H2O2) or 2,3-dimethoxy-1,4-naphthoquinone (DMNQ). Different kinds of CM-CG action were studied by two different treatment protocols: a. pre-incubation of freshly isolated hepatocytes with the potential anti-mutagen followed by exposure to the oxidant or b. simultaneous treatment of hepatocytes with the potential anti-mutagen and the oxidant., Methods: As a measure of genotoxicity, the percentages of DNA in tails of comets by single cell gel electrophoresis were evaluated. The cytotoxicological endpoints analysed were the cell density (number of cells/cm2), and the percentages of apoptotic and necrotic cells., Results: H2O2 and DMNQ, causing DNA single-strand breaks via the formation of *OH radicals, have been demostrated to induce both genotoxic and cytotoxic effects in primary rat hepatocytes resulting in increased percentages of DNA in tails of comets, and increased frequencies of apoptotic and necrotic cells accompanied by a decreased cell density. Further investigations were therefore focussed on possible modifications of these parameters by CM-CG. The results obtained clearly demonstrate that CM-CG (applied before and during treatment) protects primary rat hepatocytes against the genotoxic and cytotoxic effects of oxidative stress (H2O2 or DMNQ), whereas CM-CG itself has no effect on the endpoints of genotoxicity and cytotoxicity studied., Conclusion: Our results indicate that carboxymethyl chitin-glucan represents a natural fungal polysaccharide that can inhibit the genotoxicity and cytotoxicity of experimentally induced oxidative stress in primary rat hepatocytes.