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P XIII.78 Biological monitoring of workers exposed to emissions from petroleum plants
S112
S-XI11: Identification and evaluation of environmentalmutagens, ecogenotoxicology
Ip XIII.781
Biological monitoring of worken exposed 10 emissIons from petroleum planls
Antonina Cebulska-Wasilewska'; Diana Anderson}, Ewa Ninnkowska} , Anna WierzewskaI, Ewa Kasper', Jane Anne Hughes' , Bozena Graca", and Radiation BIOlogy DepartmmtlFJ, Radzi/cowslciego 152, 31-342 KralcOw, Poland; l Collegium Medicum UJ, KrolcOw. Poland; J BIBRA International, Carshalton, Surrey, SM5 4DS. UK
Ip XIII.801
Metabolic activation of aromatic amlnes by algle
Eva Miadokova, Svetlana Podstavkova, Viera Vlekova. Andrea Slivkova, Mtrka Slaninova, Daniel Vleek. Dept . Genet .. Foe. Nat . Sci., Comenius Uniu 842 15 Bratislaoa. Slooak Republic
'
J Enuironmental
Benzene is considered to be a human carcinogen, is clastogenic to rodents and humans, and it affects the immune response. We present here some of the results from research on genotoxicity to hutnan cells of benzene related compounds. Blood samples from twenty-four workersfrom petroleum plants, 3S unexposed controls, and 31 untreared lung cancer patients of a SImilar socso-eccnormc status and from the same region in Poland were examined for cytogenetic effects and p21cas protems levels, and for any relation to confounding factors (e.g. smoking habit, sex, familycancer history and seasonal influence). Peripheral blood was exammed, for chromosome aberrations (eA), sister chromatid exchanges (SCE), high frequency cells (HFC) and proliferative rate index (PRJ) and plasma for presence of p2l ras proteins. These parameters were used as biomarkers of genotoxic anomalies. Results showed that the occupationally exposed group had statistically significant increases in CA, and percent of aberrant cells. There were no differences between exposed and unexposed groups in SCE, HFC, PRIor the levels of cas p21 proteins. Smoking was found to affect stansucally significantly the levels of CA, percent of aberrant cells, SCE, HFC and p21 proteins. Sister chromatid exchanges were also significantly sex dependent. There were no significant differences for CA, percent aberrant cells, SCE, HfC or p21 protem levels in subgroups characterized according to cancer cases reported in the immediate family.The non-smokinggroup also showed SIgnificant increases in cytogemc damage with exposure. Results from the studies of cancer patients group showed that all types of CA (including and excluding gaps), percent of aberrant cells, SCE and cas p21 proteins were statistically significantly higher in cancer patients than in healthy donors. Although there were smaller numbers of females in the cancer patients group who were older than the males, there was a difference due to sex with significant increases in females for CA, SCE and HFC, but there was no increase for p21 proteins. None of cytogenetic damage was related to other cancers in the immediate families. All major chromosome aberration parameters differed significantly between smokers and non-smokers. A multivariate regression analysis confirmed a significant casual association between cytogenetic damage and exposure to benzene related compounds, and between cytogenetic damage, p21ras proteins and cancer as well. In conclusion, In this study cytogenetic damage and p21ras proteins appear to be associated with cancer biomarkers of genetoxic exposures. Smoking and other factors such as age and sex can have an impact on them.
IP XIII.79\
Genetic effects of high and low exposure to heavy metals
Ase Kmkje, Chris Bingham, Cecilie 0stby. Department of Botany; Norwegian University of Science and Technology, 7055 Draguoll , Norway The study alms at investigating the genotoxic effects of heavy metals on plants and small mammals from an area of high level of pollution. The material was collected m the Lapland Biospheric Reserve, in the Kola Peninsula, Russia. The study area in the reserve is about S 000 km2, and stretches from the part where the ecosystem is completely destroyed and into the area which seems to be untouched by pollutants. In this area the Severonickel Smelter Complex is the only local source of atmospheric industrialpollution. Emissions from the SeveronickelSmelter complex include 4 000 tons nickel and 4 000 tons copper annually. Levelsof metals have been measuredin plant species and tissues from small mammals. The frequency of chromosome aberrations was examined in lymphocytes from Clethrionomys rufocanus (greyside mouse) and in root-tips from Picea abies (spruce) to study the effect of pollution on cell division. The results suggest that genotcxic compounds from the environment are absorbed in plant and animal species e.g., P. abies and CI. rufocanus, the effect of which can be registered in the form of chromosome aberrations in root-tips and lymphocytes.
Aromatic amines belong to the widely spread promutagenslprocarcinogens. Althoughbiotransformationof some aromatic amines was proved in some intact plants and in the plant celUmicrobe comcubation assay in the representatives of acquatic lower plants - algae it has not been investigated yet. Repairdeficient strains of the unicellular green alga Chlamydomonas reinhard/il were used to compare the toxic and mutagenic effects of three phenylenedrarrune Isomers (meta-, ortho-, para-phenylenediamine = m-PDA, o-PDA, p-PDA), employing streptomycin - resistant mutations as genetic endpoints. It was proved that mtact algal cells acuvated promutagens used, so that they can be employed as suitable biomarkers for promutagenslprocarcanogens detection, mainly In acquatic environments. On purpose to separate the acnvatmg system and the genetic indicator system the algal/cell coincubation assay was used. Algal cells were employed as the bioacuvaung system and bactena Salmonella typhimurium TA98 and YG1024 (derivative of TA98 with increased level of O-acetyltransferase)as genetic indicator organisms. Among three Isomers used the higher activation in m-PDA was scored. Keyword(s}: Algal promutagens activation; Repair-deficient
strains;
Salmonella typhimurium
Ip XII 1.81 I
D1rrenntlal tissue distribution of DNA ad ducts In rats
exposed to sldestream elgareUe smoke C. Gary Gairola, Jamal M. Arif, Ramesh C. Gupta. THRI and Preventive Med icine. University of Kentuc ky; Lexington , KY. USA
Various studies including our's have shown that exposure to tobacco smoke induces forma tion of DNA adducts in the lungs of experimental animals. The present study was carried out to examine the distribution of DNA adducts in various tissues of rats following inhalation exposure to cigarette smoke and to determine if any of these adducts resemble benzo(a)pyrene diolepoxide (BPDE)-DNA adduct. A group of female rats was exposed daily to srdestream cigarettesmokein a whole-body exposurechamber and another age-matched controlgroup was maintainedon filteredair. Few additional rats were given a single dose of BP (I.S mglkg). After sacrifice, lungs, heart, trachea, bladder and mammary tissue were analysed for DNA adducts by )2P-postlabeling assay. The results showed that cigarette smoke exposure differentially enhanced the magnitude of DNA adducts in various tissues. Thus, adduct #S was intensified in the lungs and heart, #3 in trachea, #2 in bladder and # I in mammary glands. Adduionally, the yield of smokerelated DNA adducts was significantly greater with nuclease PI compared to butanol extraction procedure. None of the smoke-related adduets showed exact chromatographic identity to the BPDE-DNA adduct whieh was easily detectable in various tissues of BP-treated rats. The above results suggest that PAH interactions with cellular DNA may not be the main source of smoke-related DNA adducts in rats. Keyword(s): CIgarette smoke; DNA adducts; rat tissues
Ip XII1.821
Mulagenlclty of d02 urine extracts by the ultra-low micro suspenslon assay
Yukihiko Takagi' , Osamu Endo}, Sunuo Got02, Yukio Kato", Choji KaneuchiI, Ken-ichi KohzakiI . J Azabu University, Kanagawa, Japan ; 1NIPH,
Tokyo; Japan
There are a number of carcinogenic or mutagenic chemical substances in the food and environment, and an increasing number of cancer cases among household dogs has been reported in recent years. Therefore, we have investigated the mutagenicity of dog urine extracts by high sensitive mutagemeity method.
S-XI11: Identification and evaluation of environmentalmutagens, ecogenotoxicology
Ip XIII.781
Biological monitoring of worken exposed 10 emissIons from petroleum planls
Antonina Cebulska-Wasilewska'; Diana Anderson}, Ewa Ninnkowska} , Anna WierzewskaI, Ewa Kasper', Jane Anne Hughes' , Bozena Graca", and Radiation BIOlogy DepartmmtlFJ, Radzi/cowslciego 152, 31-342 KralcOw, Poland; l Collegium Medicum UJ, KrolcOw. Poland; J BIBRA International, Carshalton, Surrey, SM5 4DS. UK
Ip XIII.801
Metabolic activation of aromatic amlnes by algle
Eva Miadokova, Svetlana Podstavkova, Viera Vlekova. Andrea Slivkova, Mtrka Slaninova, Daniel Vleek. Dept . Genet .. Foe. Nat . Sci., Comenius Uniu 842 15 Bratislaoa. Slooak Republic
'
J Enuironmental
Benzene is considered to be a human carcinogen, is clastogenic to rodents and humans, and it affects the immune response. We present here some of the results from research on genotoxicity to hutnan cells of benzene related compounds. Blood samples from twenty-four workersfrom petroleum plants, 3S unexposed controls, and 31 untreared lung cancer patients of a SImilar socso-eccnormc status and from the same region in Poland were examined for cytogenetic effects and p21cas protems levels, and for any relation to confounding factors (e.g. smoking habit, sex, familycancer history and seasonal influence). Peripheral blood was exammed, for chromosome aberrations (eA), sister chromatid exchanges (SCE), high frequency cells (HFC) and proliferative rate index (PRJ) and plasma for presence of p2l ras proteins. These parameters were used as biomarkers of genotoxic anomalies. Results showed that the occupationally exposed group had statistically significant increases in CA, and percent of aberrant cells. There were no differences between exposed and unexposed groups in SCE, HFC, PRIor the levels of cas p21 proteins. Smoking was found to affect stansucally significantly the levels of CA, percent of aberrant cells, SCE, HFC and p21 proteins. Sister chromatid exchanges were also significantly sex dependent. There were no significant differences for CA, percent aberrant cells, SCE, HfC or p21 protem levels in subgroups characterized according to cancer cases reported in the immediate family.The non-smokinggroup also showed SIgnificant increases in cytogemc damage with exposure. Results from the studies of cancer patients group showed that all types of CA (including and excluding gaps), percent of aberrant cells, SCE and cas p21 proteins were statistically significantly higher in cancer patients than in healthy donors. Although there were smaller numbers of females in the cancer patients group who were older than the males, there was a difference due to sex with significant increases in females for CA, SCE and HFC, but there was no increase for p21 proteins. None of cytogenetic damage was related to other cancers in the immediate families. All major chromosome aberration parameters differed significantly between smokers and non-smokers. A multivariate regression analysis confirmed a significant casual association between cytogenetic damage and exposure to benzene related compounds, and between cytogenetic damage, p21ras proteins and cancer as well. In conclusion, In this study cytogenetic damage and p21ras proteins appear to be associated with cancer biomarkers of genetoxic exposures. Smoking and other factors such as age and sex can have an impact on them.
IP XIII.79\
Genetic effects of high and low exposure to heavy metals
Ase Kmkje, Chris Bingham, Cecilie 0stby. Department of Botany; Norwegian University of Science and Technology, 7055 Draguoll , Norway The study alms at investigating the genotoxic effects of heavy metals on plants and small mammals from an area of high level of pollution. The material was collected m the Lapland Biospheric Reserve, in the Kola Peninsula, Russia. The study area in the reserve is about S 000 km2, and stretches from the part where the ecosystem is completely destroyed and into the area which seems to be untouched by pollutants. In this area the Severonickel Smelter Complex is the only local source of atmospheric industrialpollution. Emissions from the SeveronickelSmelter complex include 4 000 tons nickel and 4 000 tons copper annually. Levelsof metals have been measuredin plant species and tissues from small mammals. The frequency of chromosome aberrations was examined in lymphocytes from Clethrionomys rufocanus (greyside mouse) and in root-tips from Picea abies (spruce) to study the effect of pollution on cell division. The results suggest that genotcxic compounds from the environment are absorbed in plant and animal species e.g., P. abies and CI. rufocanus, the effect of which can be registered in the form of chromosome aberrations in root-tips and lymphocytes.
Aromatic amines belong to the widely spread promutagenslprocarcinogens. Althoughbiotransformationof some aromatic amines was proved in some intact plants and in the plant celUmicrobe comcubation assay in the representatives of acquatic lower plants - algae it has not been investigated yet. Repairdeficient strains of the unicellular green alga Chlamydomonas reinhard/il were used to compare the toxic and mutagenic effects of three phenylenedrarrune Isomers (meta-, ortho-, para-phenylenediamine = m-PDA, o-PDA, p-PDA), employing streptomycin - resistant mutations as genetic endpoints. It was proved that mtact algal cells acuvated promutagens used, so that they can be employed as suitable biomarkers for promutagenslprocarcanogens detection, mainly In acquatic environments. On purpose to separate the acnvatmg system and the genetic indicator system the algal/cell coincubation assay was used. Algal cells were employed as the bioacuvaung system and bactena Salmonella typhimurium TA98 and YG1024 (derivative of TA98 with increased level of O-acetyltransferase)as genetic indicator organisms. Among three Isomers used the higher activation in m-PDA was scored. Keyword(s}: Algal promutagens activation; Repair-deficient
strains;
Salmonella typhimurium
Ip XII 1.81 I
D1rrenntlal tissue distribution of DNA ad ducts In rats
exposed to sldestream elgareUe smoke C. Gary Gairola, Jamal M. Arif, Ramesh C. Gupta. THRI and Preventive Med icine. University of Kentuc ky; Lexington , KY. USA
Various studies including our's have shown that exposure to tobacco smoke induces forma tion of DNA adducts in the lungs of experimental animals. The present study was carried out to examine the distribution of DNA adducts in various tissues of rats following inhalation exposure to cigarette smoke and to determine if any of these adducts resemble benzo(a)pyrene diolepoxide (BPDE)-DNA adduct. A group of female rats was exposed daily to srdestream cigarettesmokein a whole-body exposurechamber and another age-matched controlgroup was maintainedon filteredair. Few additional rats were given a single dose of BP (I.S mglkg). After sacrifice, lungs, heart, trachea, bladder and mammary tissue were analysed for DNA adducts by )2P-postlabeling assay. The results showed that cigarette smoke exposure differentially enhanced the magnitude of DNA adducts in various tissues. Thus, adduct #S was intensified in the lungs and heart, #3 in trachea, #2 in bladder and # I in mammary glands. Adduionally, the yield of smokerelated DNA adducts was significantly greater with nuclease PI compared to butanol extraction procedure. None of the smoke-related adduets showed exact chromatographic identity to the BPDE-DNA adduct whieh was easily detectable in various tissues of BP-treated rats. The above results suggest that PAH interactions with cellular DNA may not be the main source of smoke-related DNA adducts in rats. Keyword(s): CIgarette smoke; DNA adducts; rat tissues
Ip XII1.821
Mulagenlclty of d02 urine extracts by the ultra-low micro suspenslon assay
Yukihiko Takagi' , Osamu Endo}, Sunuo Got02, Yukio Kato", Choji KaneuchiI, Ken-ichi KohzakiI . J Azabu University, Kanagawa, Japan ; 1NIPH,
Tokyo; Japan
There are a number of carcinogenic or mutagenic chemical substances in the food and environment, and an increasing number of cancer cases among household dogs has been reported in recent years. Therefore, we have investigated the mutagenicity of dog urine extracts by high sensitive mutagemeity method.