Mouse skin tumor initiation-promotion and complete carcinogenesis bioassays: mechanisms and biological activities of emission samples.

نویسندگان

  • S Nesnow
  • L L Triplett
  • T J Slaga
چکیده

Extracts of soots obtained from various sources were applied to the skin of mice in an effort to identify carcinogens in these mixtures and to link these materials to the etiology of human cancer. Samples of coal chimney soot, coke oven materials, industrial carbon black, oil shale soot, and gasoline vehicle exhaust materials have been examined by this method. The studies reported here have been constructed to compare the carcinogenic and tumorigenic potency of extracts from various particulate emissions: coke ovens, diesel and gasoline vehicles and a roofing tar pot. Automobile emission samples were obtained by collecting the diluted and cooled exhaust on Teflon-coated glass fiber filters. Coke oven and roofing tar samples were particulate emission samples collected by impaction and filtration. The organic components associated with each of the particles were extracted with dichloromethane and dermally applied to SENCAR mice. All agents were applied as tumor initiators by using a five-dose protocol. Selected extracts were also applied as complete carcinogens and as tumor promotors. Statistical analyses of the resulting tumor data were performed by using nonlinear Poisson and probit models. The results from these experiments provide a suitable data base for comparative potency estimation of complex mixtures.

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

Protective effects of silymarin against photocarcinogenesis in a mouse skin model.

BACKGROUND Nonmelanoma skin cancer is the most common cancer among humans; solar UV is its major cause. Therefore, it is important to identify agents that can offer protection against this cancer. PURPOSE We evaluated the protective effects of silymarin, a flavonoid compound isolated from the milk thistle plant, against UVB radiation-induced nonmelanoma skin cancer in mice and delineated the ...

متن کامل

EFFECT OF IRON OVERLOAD ON 7, 12-DIMETHYLBENZ (A) ANTHRACENE-INDUCED SKIN TUMORIGENESIS

Iron overload is known to occur in the West European and American population due to the consumption of iron-rich diets. On the other hand, genetic disorders leading to iron overload are also known. Iron overload leads to increased peroxidation and disruptive disintegration of lipid-rich membranes, and predisposes humans for an enhanced risk of cancer induction. In experimental animals iron ...

متن کامل

Differential Effects of Retinoic Acid and 7,8-Benzoflavone on the Induction of Mouse Skin Tumors by the Complete Carcinogenesis Process and by the Initiation-Promotion Regimen1

The present study was designed to elucidate differences in the mechanism of the induction of mouse skin tumors either by the initiation-promotion regimen or by the complete carcinogenesis process. The protocols used to elicit skin tumors were: (a) by the initiation-promotion regimen, a single application of 0.2 ,umol of 7,12-dimethylbenz[a]anthracene (DMBA) followed by twice-weekly applications...

متن کامل

Inhibition of tumor promoter-induced ornithine decarboxylase activity by tannic acid and other polyphenols in mouse epidermis in vivo.

Naturally occurring plant phenols with antimutagenic and anticarcinogenic activities were tested for their abilities to inhibit the ornithine decarboxylase (ODC) response linked to skin tumor promotion by 12-O-tetradecanoylphorbol-13-acetate (TPA). Topical applications of tannic acid (TA) inhibit remarkably and in a dose-dependent manner TPA-induced ODC activity in mouse epidermis in vivo. This...

متن کامل

Error-prone translesion replication of damaged DNA suppresses skin carcinogenesis by controlling inflammatory hyperplasia.

The induction of skin cancer involves both mutagenic and proliferative responses of the epidermis to ultraviolet (UV) light. It is believed that tumor initiation requires the mutagenic replication of damaged DNA by translesion synthesis (TLS) pathways. The mechanistic basis for the induction of proliferation, providing tumor promotion, is poorly understood. Here, we have investigated the role o...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

عنوان ژورنال:
  • Environmental Health Perspectives

دوره 47  شماره 

صفحات  -

تاریخ انتشار 1983