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1

Study of arsenic exposure in oral/oropharyngeal carcinoma in West Bengal

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Pal P., Raychowdhury R., Dolai T. K., Roy S., Dastidar R., Halder A.

International Journal of Occupational Medicine and Environmental Health

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2017

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vol. 30

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issue 2

271-279

EN

Objectives To study any possible correlation between arsenic toxicity and the development of oral carcinoma in West Bengal population. Material and Methods Ethical clearance for this study was obtained from the Vivekananda Institute of Medical Sciences. Out of 30 785 patients attending our hospital from November 2012 to July 2015, 107 cases and 50 control individuals were selected. The hair and buccal smear samples were obtained upon their consent for the purpose of the analysis of arsenic count and cytogenetic damage, respectively. Results Ninety-six percent of cases came from the highly arsenic affected districts and 81.3% showed their arsenic count above the safe limit (0.8 μg/g) whereas 96% of the controls’ arsenic count was within the safe limit. The study showed a significant difference of the micronuclei and apoptosis frequency between the cases and controls. Conclusions The difference of micronuclei and apoptosis frequency between cases and controls was significant. The maximum number of cases came from highly arsenic affected areas and a higher percentage of cases showed elevated arsenic count, as compared to controls, which may indicate a possible link between arsenic toxicity and this disease. However, a larger sample size is required for a proper correlation. Int J Occup Med Environ Health 2017;30(2):271–279

2

Lipopolysaccharide accelerates fine particulate matter-induced cell apoptosis in human lung bronchial epithelial cells

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Ru Q., Xiong Q., Chen L., Tian X., Yue K., Ma B., Liu L., Wu R., Xu C., Pi M., Li C.

International Journal of Occupational Medicine and Environmental Health

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2017

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vol. 31

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issue 2

173-183

EN

Objectives The aim of the study has been to investigate the effect of the Standard Reference Material of fine particulate matter (SRM 2786) on cytotoxicity and apoptosis in human lung bronchial epithelial cells (16HBE cells). Whether the lipopolysaccharide (LPS)-induced inflammation could further accelerate cell apoptosis induced by SRM 2786 stimulation has also been determined. Material and Methods 16HBE cells were exposed to various doses of SRM 2786 with or without LPS. The following parameters: cytotoxicity, apoptotic rate, Bax/Bcl-2 expression, nitric oxide (NO) production, and reactive oxygen species (ROS) generation were measured. Results The results have shown that SRM 2786 induces cell damage and apoptosis of 16HBE cells as demonstrated by significant decrease in expression of Bcl-2 and increase in expression of Bax. When compared with the control cells, the apoptotic rate of cells treated by 500 μg/ml of SRM 2786 increased from 2.43±0.21% to 43.96±2.95% (p < 0.01). Further, there was an elevated production of NO and ROS post SRM 2786 treatment. The level of NO in cells treated with 500 μg/ml of SRM 2786 was 18.33±1.02 μmol/l whereas that of control cells was 1.58±0.31 μmol/l (p < 0.01). When compared with the control group, the level of intracellular ROS increased by 24% after treatment with 500 μg/ml of SRM 2786 (p < 0.05). In addition, LPS pre-treatment may accelerate cell apoptosis by increasing generation of NO and ROS followed by SRM 2786 stimulation. When compared to cells treated with 125 μg/ml of SRM 2786 alone, the levels of NO and ROS in cells pretreated with LPS increased by 28% and 11.6%, respectively (p < 0.05), and the apoptotic rate increased from 34.62±4.44% to 54.11±3.34% (p < 0.01). Conclusions These findings have suggested that in vitro exposure to SRM 2786 could induce 16HBE cells apoptosis probably by means of the mechanism involving the generation of free radicals, while the degree of apoptosis would be further aggravated under inflammation condition. Int J Occup Med Environ Health 2018;31(2):173–183

3

Oxidative stress and apotosis to zebrafish (Danio rerio) embryos exposed to perfluorooctane sulfonate (PFOS) and ZnO nanoparticles

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Du J., Cai J., Wang S., You H.

International Journal of Occupational Medicine and Environmental Health

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2017

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vol. 30

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issue 2

213-229

EN

Objectives Perfluorooctane sulfonate (PFOS) and zinc oxide nanoparticles (ZnO-NPs) are frequently detected in the environment but few studies have assessed the joint toxicity of them. Oxidative stress and apoptosis to zebrafish (Danio rerio) embryos induced by the PFOS and ZnO-NPs were investigated in this study. Material and Methods The embryos were exposed to the PFOS (0, 0.4, 0.8 and 1.6 mg/l), ZnO-NPs (12.5, 25, 50 mg/l) and PFOS plus ZnO-NPs (0.4+12.5, 0.8+25 and 1.6+50 mg/l) mixture solutions until 96 h post-fertilization. Activities of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (Gpx) and malondialdehyde (MDA) content were measured in zebrafish embryos after exposure lasting for 96 h. At the same time, the genes expression related to reactive oxygen species (ROS) generation, oxidative damage and apoptosis were also measured. Results A significant induction of the ROS accompanied by the increase in the activity of the Gpx and MDA contents were found in co-treatment groups. Furthermore, several apoptosis pathway related genes such as Bax, p53, caspase-3 and caspase-9 were significantly up-regulated in the PFOS plus ZnO-NPs exposure groups, while anti-apoptotic gene Bcl-2 was significantly down-regulated in the PFOS plus ZnO-NPs exposure groups. In addition, some oxidative stress-related genes such as Cat, GSH peroxidase 1 (Gpx1a) and superoxide dismutase 1 (Sod1) were also significantly down-regulated after the PFOS plus ZnO-NPs co-treatments. Conclusions The results demonstrated that the PFOS plus ZnO-NPs co-exposure could cause more serious oxidative stress and apoptosis than the PFOS and ZnO-NPs exposure alone at the exposure concentrations above. The synergistic effects of the PFOS and ZnO-NPs may be the important mechanisms of their toxicity to zebrafish embryos. Int J Occup Med Environ Health 2017;30(2):213–229

4

Attenuating effects of caffeic acid phenethyl ester with intralipid on hepatotoxicity of chlorpyrifos in the case of rats

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Dokuyucu R., Bilgili A., Hanedan B., Dogan H., Dokuyucu A., Celik M. M.

Medycyna Pracy

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2016

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vol. 67

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issue 6

743-749

PL

Wstęp Chloropiryfos (CPF), środek owadobójczy szeroko stosowany w rolnictwie, może powodować zatrucia u ludzi. Z tego powodu prowadzi się wiele badań dotyczących możliwości leczenia zatrucia chloropiryfosem. Celem pracy była ocena wpływu estru fenetylowego kwasu kawowego (caffeic acid phenethyl ester – CAPE) i intralipidu (IL) na uszkodzenia wątroby u szczurów wywołane przez chloropiryfos. Materiał i metody Szczurom podawano CPF (10 mg/kg masy ciała (mc.), doustnie), CAPE (10 μmol/kg mc., dootrzewnowo), IL (18,6 ml/kg mc., doustnie), CPF+CAPE, CPF+IL oraz CPF+CAPE+IL. Zmierzono całkowitą zdolność utleniającą (total oxidant capacity – TOC) i całkowitą zdolność przeciwutleniającą (total antioxidant capacity – TAC) osocza krwi i obliczono wskaźnik stresu oksydacyjnego (oxidative stress index – OSI). U zwierząt wykonano także badanie histopatologiczne i barwienie immunohistochemiczne tkanek wątroby. Wyniki Chloropiryfos istotnie zmniejszał u badanych szczurów TAC osocza, a zwiększał apoptozę, TOC i OSI. Natomiast CAPE i CAPE+IL istotnie zmniejszały OSI osocza i apoptozę, a zwiększały TAC osocza u szczurów z uszkodzeniami wątroby wywołanymi przez chloropiryfos. Wnioski Badanie wykazało, że CAPE i CAPE+IL poprzez zmniejszenie stresu oksydacyjnego i apoptozy redukują u szczurów uszkodzenia wątroby wywołane przez chloropiryfos. Med. Pr. 2016;67(6):743–749

EN

Background Chlorpyrifos (CPF), insecticide widely used in agriculture, may cause poisonings in the case of humans. As a result, there is a large amount of treatment research underway to focus on the possibility of chlorpyrifos induced poisonings. The aim of this study has been to evaluate the effects of caffeic acid phenethyl ester (CAPE) and intralipid (IL) on hepatotoxicity induced by chlorpyrifos in the case of rats. Material and Methods The rats in this study were treated with CPF (10 mg/kg body weight (b.w.), orally), CAPE (10 μmol/kg b.w., intraperitoneally), IL (18.6 ml/kg b.w., orally), CPF+CAPE, CPF+IL, and CPF+CAPE+IL. The plasma total oxidant capacity (TOC), total antioxidant capacity (TAC) were measured and the oxidative stress index (OSI) was calculated. Liver histopathology and immunohistochemical staining were performed. Results Chlorpyrifos statistically significantly decreased the TAC levels in the rats’ plasma and increased the apoptosis and the TOC and OSI levels. In the chlorpyrifos induced liver injury, CAPE and CAPE+IL significantly decreased the plasma OSI levels and the apoptosis, and significantly increased the plasma TAC levels. Conclusions This study revealed that CAPE and CAPE+IL attenuate chlorpyrifos induced liver injuries by decreasing oxidative stress and apoptosis. Med Pr 2016;67(6):743–749

5

Arsen – trucizna czy lek?

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Kulik-Kupka K., Koszowska A., Brończyk-Puzoń A., Nowak J., Gwizdek K., Zubelewicz-Szkodzińska B.

Medycyna Pracy

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2016

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vol. 67

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issue 1

89-96

EN

Arsenic (As) is commonly known as a poison. Only a few people know that As has also been widely used in medicine. In the past years As and its compounds were used as a medicine for the treatment of such diseases as diabetes, psoriasis, syphilis, skin ulcers and joint diseases. Nowadays As is also used especially in the treatment of patients with acute promyelocytic leukemia. The International Agency for Research on Cancer (IARC) has recognized arsenic as an element with carcinogenic effect evidenced by epidemiological studies, but as previously mentioned it is also used in the treatment of neoplastic diseases. This underlines the specificity of the arsenic effects. Arsenic occurs widely in the natural environment, for example, it is present in soil and water, which contributes to its migration to food products. Long exposure to this element may lead to liver damages and also to changes in myocardium. Bearing in mind that such serious health problems can occur, monitoring of the As presence in the environmental media plays a very important role. In addition, the occupational risk of As exposure in the workplace should be identified and checked. Also the standards for As presence in food should be established. This paper presents a review of the 2015 publications based on the Medical database like PubMed and Polish Medical Bibliography. It includes the most important information about arsenic in both forms, poison and medicine. Med Pr 2016;67(1):89–96

PL

Arsen to pierwiastek kojarzony głównie z działaniem toksycznym. Należy jednak podkreślić, że mimo toksyczności jest on stosowany w medycynie. W przeszłości arsen i jego związki wykorzystywano w leczeniu m.in. cukrzycy, łuszczycy, kiły, owrzodzeń skóry i chorób stawów. Obecnie stosowany jest w onkologii, głównie u pacjentów z ostrą białaczką promielocytową. Z jednej strony więc arsen został uznany przez Międzynarodową Agencję Badań nad Rakiem (International Agency for Research on Cancer – IARC) za pierwiastek o udowodnionym epidemiologicznie rakotwórczym działaniu, a z drugiej – jest wykorzystywany w terapii chorób onkologicznych. Na działanie arsenu człowiek jest narażony także w codziennym życiu, ponieważ jest to substancja szeroko rozpowszechniona w przyrodzie. Występuje w glebie i wodzie, co skutkuje przedostawaniem się tego związku do pożywienia. Długotrwała ekspozycja na arsen i jego związki może doprowadzić np. do zmian w mięśniu sercowym lub uszkodzenia wątroby. Z tego powodu ważne jest prowadzenie monitoringu zawartości tej substancji w glebie, wodzie i pożywieniu, a także możliwości narażenia zawodowego. Niezbędne jest także ustalenie norm zawartości tego pierwiastka (zarówno zawartości całkowitej, jak i jego nieorganicznej formy) w pożywieniu. Niniejszy artykuł jest przeglądem publikacji znajdujących się w bazach medycznych PubMed oraz Polskiej Bibliografii Lekarskiej, które ukazały się do 2015 r. oraz dotyczyły arsenu i jego związków. W artykule przedstawiono najważniejsze informacje dotyczące arsenu – zarówno jako trucizny, jak i leku. Med. Pr. 2016;67(1):89–96

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Etery glikolu etylenowego i glikolu propylenowego – toksyczność reprodukcyjna i rozwojowa

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Starek-Świechowicz B., Starek A.

Medycyna Pracy

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2015

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vol. 66

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issue 5

725-737

EN

Both ethylene and propylene glycol alkyl ethers (EGAEs and PGAEs, respectively) are widely used, mainly as solvents, in industrial and household products. Some EGAEs demonstrate gonadotoxic, embriotoxic, fetotoxic and teratogenic effects in both humans and experimental animals. Due to the noxious impact of these ethers on reproduction and development of organisms EGAEs are replaced for considerably less toxic PGAEs. The data on the mechanisms of testicular, embriotoxic, fetotoxic and teratogenic effects of EGAEs are presented in this paper. Our particular attention was focused on the metabolism of some EGAEs and their organ-specific toxicities, apoptosis of spermatocytes associated with changes in the expression of various genes that code for oxidative stress factors, protein kinases and nuclear hormone receptors. Med Pr 2015;66(5):725–737

PL

Etery alkilowe glikolu etylenowego (ethylene glycol alkyl ethers – EGAE) i propylenowego (propylene glycol alkyl ethers – PGAE) są szeroko stosowane w przemyśle i gospodarstwie domowym, głównie jako rozpuszczalniki. Niektóre EGAE wykazują działanie gonadotoksyczne, embriotoksyczne, fetotoksyczne i teratogenne zarówno u ludzi, jak i zwierząt doświadczalnych. Ze względu na szkodliwe działanie tych eterów na rozrodczość i rozwój organizmu EGAE są zastępowane znacznie mniej toksycznymi PGAE. W niniejszej pracy przedstawiono dane na temat mechanizmów toksycznego działania EGAE na komórki rozrodcze, zarodek i płód. Szczególną uwagę zwrócono na metabolizm niektórych EGAEs i ich toksyczność narządową, a także na apoptozę spermatocytów związaną ze zmianami ekspresji genów, które kodują czynniki stresu oksydacyjnego, kinazy białkowe i jądrowe receptory hormonów. Med. Pr. 2015;66(5):725–737

Refine search results

Study of arsenic exposure in oral/oropharyngeal carcinoma in West Bengal

Lipopolysaccharide accelerates fine particulate matter-induced cell apoptosis in human lung bronchial epithelial cells

Oxidative stress and apotosis to zebrafish (Danio rerio) embryos exposed to perfluorooctane sulfonate (PFOS) and ZnO nanoparticles

Attenuating effects of caffeic acid phenethyl ester with intralipid on hepatotoxicity of chlorpyrifos in the case of rats

Arsen – trucizna czy lek?

Etery glikolu etylenowego i glikolu propylenowego – toksyczność reprodukcyjna i rozwojowa