Determination of the sulphur balance in coal during combustion in small and large fuel beds

U toku ovih ispitivanja eksperimentalno smo provjeravali uobičajeni proračun emisije sumpora na osnovu tzv. »sagorivog sumpora« u uglju. Mjerenja sadržaja sumpora u dimnim plinovima su pokazala da se ovakvim proračunima, koji se baziraju na određivanju tzv. »vezanog sumpora« u laboratorijskim uslovima spaljivanjem goriva do 800°C, može načiniti greška i do 100%. Emisija sumpora iz velikih ložišta za centralno grijanje kreće se otprilike 90%, dok je pretpostavljena emisija iz podataka o »sagorivom sumporu« trebala da iznosi otprilike 50%. Emisije sumpora iz sobnih peći kretale su se od 56 do 88% zavisno od konstrukcije, te od načina loženja i režima rada peći. I u ovom su slučaju emisije redovno bile više od očekivanih emisija »sagorivog sumpora«. Rezu!tati ovih mjerenja nam pokazuju da se prilikom projektovanja i proračuna emisije i visine dimnjaka ne možemo osloniti samo na podatke o sadržaju »sagorivog sumpora« u gorivu nego na eksperimentalne podatke o bilansu sumpora, koji se sve češće mogu naći u stranoj tehničkoj literaturi.The usual rough estimate of sulphur emission was checked experimentally on the basis of the sulphur content in coal known as »burnt sulphur«. The measurements of the content of sulphur in stack gases proved that such an estimate based on the measuring of sulphur in ash known as »bound sulphur« under laboratory conditions of burning fuel up to 800°C, can result in an error of up to 100%. The emission of sulphur from solid fuel beds used for central heating comes to 90% while the supposed emission based on »burnt sulphur« should be about 50%. The sulphur emission from domestic stoves reached 56% to 88% depending on stove design, coal burning and on operating conditions. The emissions were always greater than the expected emissions of »burnt sulphur«. The results of these measurements indicate that we cannot rely only on the information concerning »burnt sulphur« content when the design and calculation of chimney emission and height is carried out, but the experimental data on sulphur balance should also be taken into account. Such data can be more and more often found in foreign technical literature

Advanced glycoxidation and lipoxidation end products (AGEs and ALEs): an overview of their mechanisms of formation

Advanced lipoxidation end products (ALEs) and advanced glycation end products (AGEs) have a pathogenetic role in the development and progression of different oxidative-based diseases including diabetes, atherosclerosis, and neurological disorders. AGEs and ALEs represent a quite complex class of compounds that are formed by different mechanisms, by heterogeneous precursors and that can be formed either exogenously or endogenously. There is a wide interest in AGEs and ALEs involving different aspects of research which are essentially focused on set-up and application of analytical strategies (1) to identify, characterize, and quantify AGEs and ALEs in different pathophysiological conditions ; (2) to elucidate the molecular basis of their biological effects ; and (3) to discover compounds able to inhibit AGEs/ALEs damaging effects not only as biological tools aimed at validating AGEs/ALEs as drug target, but also as promising drugs. All the above-mentioned research stages require a clear picture of the chemical formation of AGEs/ALEs but this is not simple, due to the complex and heterogeneous pathways, involving different precursors and mechanisms. In view of this intricate scenario, the aim of the present review is to group the main AGEs and ALEs and to describe, for each of them, the precursors and mechanisms of formation

DNA damage by lipid peroxidation products: implications in cancer, inflammation and autoimmunity

Oxidative stress and lipid peroxidation (LPO) induced by inflammation, excess metal storage and excess caloric intake cause generalized DNA damage, producing genotoxic and mutagenic effects. The consequent deregulation of cell homeostasis is implicated in the pathogenesis of a number of malignancies and degenerative diseases. Reactive aldehydes produced by LPO, such as malondialdehyde, acrolein, crotonaldehyde and 4-hydroxy-2-nonenal, react with DNA bases, generating promutagenic exocyclic DNA adducts, which likely contribute to the mutagenic and carcinogenic effects associated with oxidative stress-induced LPO. However, reactive aldehydes, when added to tumor cells, can exert an anticancerous effect. They act, analogously to other chemotherapeutic drugs, by forming DNA adducts and, in this way, they drive the tumor cells toward apoptosis. The aldehyde-DNA adducts, which can be observed during inflammation, play an important role by inducing epigenetic changes which, in turn, can modulate the inflammatory process. The pathogenic role of the adducts formed by the products of LPO with biological macromolecules in the breaking of immunological tolerance to self antigens and in the development of autoimmunity has been supported by a wealth of evidence. The instrumental role of the adducts of reactive LPO products with self protein antigens in the sensitization of autoreactive cells to the respective unmodified proteins and in the intermolecular spreading of the autoimmune responses to aldehyde-modified and native DNA is well documented. In contrast, further investigation is required in order to establish whether the formation of adducts of LPO products with DNA might incite substantial immune responsivity and might be instrumental for the spreading of the immunological responses from aldehyde-modified DNA to native DNA and similarly modified, unmodified and/or structurally analogous self protein antigens, thus leading to autoimmunity

Biocompatibility of oxygen-plasma-treated polystyrene substrates

The biocompatibility of polystyrene (PS) samples has been improved by treatment with weakly ionized highly non-equilibrium oxygen plasma. Samples were exposed to plasma for 30 s for which they have received a dose of ions of 4.5 × 1017 m−2 and a neutral oxygen atom dose of 3 × 10−23 m−2. Both untreated and plasma-treated samples were tested for biocompatibility according to the same procedure. Proliferation of human mammary epithelial cells (HMECs) on samples revealed a dramatically improved biocompatibility of polystyrene treated by oxygen plasma. The HMECs were deposited on all samples and incubated for 1, 2 and 6 days. MTT test revealed about two times higher activity of cell enzymes after 48 h incubation. The activity for plasma-treated samples remained much higher than for untreated samples even after 6 days of incubation when the samples were already covered with a dense film of HMECs

Combined metformin and insulin treatment reverses metabolically impaired omental adipogenesis and accumulation of 4-hydroxynonenal in obese diabetic patients

OBJECTIVE: Obesity-associated impaired fat accumulation in the visceral adipose tissue can lead to ectopic fat deposition and increased risk of insulin resistance and type 2 diabetes mellitus (T2DM). This study investigated whether impaired adipogenesis of omental (OM) adipose tissues and elevated 4-hydroxynonenal (4-HNE) accumulation contribute to this process, and if combined metformin and insulin treatment in T2DM patients could rescue this phenotype. ----- METHODS: OM adipose tissues were obtained from forty clinically well characterized obese individuals during weight reduction surgery. Levels of 4-HNE protein adducts, adipocyte size and number of macrophages were determined within these tissues by immunohistochemistry. Adipogenic capacity and gene expression profiles were assessed in preadipocytes derived from these tissues in relation to insulin resistance and in response to 4-HNE, metformin or combined metformin and insulin treatment. ----- RESULTS: Preadipocytes isolated from insulin resistant (IR) and T2DM individuals exhibited lower adipogenesis, marked by upregulation of anti-adipogenic genes, compared to preadipocytes derived from insulin sensitive (IS) individuals. Impaired adipogenesis was also associated with increased 4-HNE levels, smaller adipocytes and greater macrophage presence in the adipose tissues. Within the T2DM group, preadipocytes from combined metformin and insulin treated subset showed better in vitro adipogenesis compared to metformin alone, which was associated with less presence of macrophages and 4-HNE in the adipose tissues. Treatment of preadipocytes in vitro with 4-HNE reduced their adipogenesis and increased proliferation, even in the presence of metformin, which was partially rescued by the presence of insulin. ----- CONCLUSION: This study reveals involvement of 4-HNE in the impaired OM adipogenesis-associated with insulin resistance and T2DM and provides a proof of concept that this impairment can be reversed by the synergistic action of insulin and metformin. Further studies are needed to evaluate involvement of 4-HNE in metabolically impaired abdominal adipogenesis and to confirm benefits of combined metformin-insulin therapy in T2DM patients

Determination of multiple mycotoxins in Qatari population serum samples by LC-MS/MS

Human exposure to mycotoxins is almost inevitable as mycotoxins are naturally occurring contaminants of large portion of food and feed. Depending on the type of mycotoxins, inter-individual mycotoxin adsorption, bioaccumulation, distribution, metabolism and excretion, can cause serious adverse health effects. Therefore, continuous biomonitoring studies of population exposure to mycotoxins are needed. Here we describe a multi-analyte approach for the detection and quantification of 20 mycotoxins in human serum using ultra-performance liquid chromatography-electrospray/tandem mass spectrometry operated in targeted multiple reaction monitoring mode. The validated method was used to assess occurrence of mycotoxins in serum samples of 46 residents of Qatar. Mycotoxins that were detected with high incidence were HT-2 toxin (13.0%), sterigmatocystin (10.9%) and 3-acetyldeoxynivalenol (6.5%). Also, co-exposure to several mycotoxins was noticed in the analysed samples. Our results show that strict food quality control is needed to remove mycotoxin contaminated food from the market in order to minimise human exposure to mycotoxins