Wyznaczanie parametrów toksykologicznych wybranych organicznych substancji bioaktywnych z zastosowaniem testu Ostracodtoxkit FTM

Assessment of the impact of pharmaceutical residues on living organisms is very complex subject. Apart from taking into account the toxicity of individual compounds also their presence in mixtures should be taken into account. In this work, attempts were made to assess the ecotoxicity of biologically active substances (with 50 % effective concentration (EC50) values growing from fluoxetine (EC50 = 4.431 nM) >> gemfibrozil ≈ 17α-ethinylestradiol ≈ ketorolac > indomethacin > theophylline ≈ progesterone > naproxen ≈ trypsin > 2-(2,4,5-trichlorophenoxy)propionic acid > chloramphenicol > acetylsalicylic acid > ibuprofen > ketoprofen > 19-norethindrone to bezafibrate as the least toxic drug among studied ones) to the ISO standardized Ostracodtoxkit FTM bioassay. The Ostracodtoxkit FTM was proven to be very sensitive tool with respect to responding to presence of pharmaceuticals. Results of studies justify the statement that more research is needed in field of assessment of chronic exposure to pharmaceuticals and other newly emerging pollutants especially when they are present in complex mixture.Ocena wpływu pozostałości farmaceutyków na organizmy żywe jest bardzo złożonym zagadnieniem. Oprócz brania pod uwagę toksyczności tylko pojedynczych związków również współobecność wielu zanieczyszczeń musi być rozważana. W niniejszej pracy podjęto próbę wyznaczenia stopnia ekotoksyczności biologicznie aktywnych substancji (o wartościach stężeń efektywnych (EC50) rosnących w szeregu fluoksetyna (EC50 = 4.431 nM) >> gemfibrozyl ≈ 17α-etynyloestradiol≈ketorolak > indometacyna > teofilina ≈ progesteron > naproksen ≈ trypsyna > kwas 2-(2,4,5-trichlorofenoksy)propionowy > chloramfenikol > kwas acetylosalicylowy > ibuprofen > ketoprofen > 19-noretyndron ≈ bezafibrat jako najmniej toksyczny lek pośród badanych) wobec testu Ostracodtoxkit FTM, standaryzowanego normą ISO. Test Ostracodtoxkit FTM okazał się bardzo czułym narzędziem pod względem odpowiedzi na obecność farmaceutyków. Wyniki badań uzasadniają stwierdzenie, że więcej badań jest koniecznych do przeprowadzenia w obszarze oceny ekspozycji chronicznej na farmaceutyki i inne nowo pojawiające się zanieczyszczenia, zwłaszcza w przypadku ich obecności w złożonych mieszaninach

The potential interaction of environmental pollutants and circadian rhythm regulations that may cause leukemia

Tumor suppressor genes are highly affected during the development of leukemia, including circadian clock genes. Circadian rhythms constitute an evolutionary molecular machinery involving many genes, such as BMAL1, CLOCK, CRY1, CRY2, PER1, PER2, REV-ERBa, and RORA, for tracking time and optimizing daily life during day-night cycles and seasonal changes. For circulating blood cells many of these genes coordinate their proliferation, output, and function, and therein lies their importance for the development of leukemia. Recent findings suggest that environmental pollutants may affect circadian rhythms and thus affect cancer development and treatment. Such environmental pollutants are often found in mixtures and include benzene, tobacco smoke, pesticides and microplastics. Our understanding of the molecular basis for the interaction mechanisms within complex mixtures is also growing, confirming the plausible occurrence of synergistic (superadditive effect) and antagonistic (cancellation effect) actions of pollutant cocktails. In this work, we discuss the relationship of environmental pollutants and the alteration of circadian rhythms that potentially may cause leukemia. We highlight the need of additional dimensions and perhaps a paradigm shift for future studies in relation to continuously growing magnitude of environmental pollution using multitude of disciplines such as development of high throughput reporter cell lines, other cell screening methods, contaminant measurements in leukemia patients, advanced pharmacology and toxicological measurement of mixtures and highly efficient computer analysis including artificial intelligence, among others

N-way modelling of sediment monitoring data from Mar Menor lagoon, Spain

The present paper deals with the application of Tucker3 modelling to a sediment monitoring data set from the area of Mar Menor coastal lagoon (Spain). The aim of the study is to model and interpret the fractionation of heavy metals in the suspended particulate matter and sediment fractions resulting by sedimentation processes. Since the lagoon is seriously influenced by anthropogenic activities the modelling aims an assessment of the environmental hazard, too. After application of various scaling and centering procedures and estimation of the model dimensionality, an optimal (3, 3, 3) Tucker3 model was chosen for data interpretation. Using the model output (factor loadings connected to the four main core elements) it could be concluded that the heavy metal concentrations in the suspended particulate matter and sediment fractions increase in order Cu > Mn > Zn ≈ Pb > Cd and could be examined as estimation of basic levels for all heavy metals caused by different sedimentation processes. The second important core element summarizes the anthropogenic influence of the mining activity in the region. The third important core element shows the different mobility of the heavy metals. The fourth important core element should be related to the specific sediment formation at one of the sampling location. © 2009 Elsevier B.V. All rights reserved

Role of the synergistic interactions of environmental pollutants in the development of cancer

There is a growing awareness that the large number of environmental pollutants we are exposed to on a daily basis are causing major health problems. Compared to traditional studies that focus on individual pollutants, there are relatively few studies on how pollutants mixtures interact. Several studies have reported a relationship between environmental pollutants and the development of cancer, even when pollutant levels are below toxicity reference values. The possibility of synergistic interactions between different pollutants could explain how even low concentrations can cause major health problems. These intricate that molecular interactions can occur through a wide variety of mechanisms, and our understanding of the physiological effects of mixtures is still limited. The purpose of this paper is to discuss recent reports that address possible synergistic interactions between different types of environmental pollutants that could promote cancer development. Our literature studies suggest that key biological pathways are frequently implicated in such processes. These include increased production of reactive oxygen species, activation by cytochrome P450, and aryl hydrocarbon receptor signaling, among others. We discuss the need to understand individual pathological vulnerability not only in relation to basic genetics and gene expression, but also in terms of measurable exposure to contaminants. We also mention the need for significant improvements in future studies using a multitude of disciplines, such as the development of high-throughput study models, better tools for quantifying pollutants in cancer patients, innovative pharmacological and toxicological studies, and high-efficiency computer analysis, which allow us to analyze the molecular mechanisms of mixtures. Plain Language Summary In general, every day we are exposed to many pollutants at the same time, and each pollutant can interact with others in different ways. Notably, two or more pollutants can interact and enhance their effects through a phenomenon called synergy and this would explain why, even at low concentrations, pollutants can have important health effects. Several studies have reported a link between environmental pollutants and cancer. Thus, our review of the literature suggests that synergy phenomena between pollutants can alter key points in cells and facilitate cancer development. Similarly, we mention the complications and needs to assess these complex interactions in subsequent studies.De två första författarna delar förstaförfattarskapetI publikationen är två av författarnas namn felstavade</p