Processing results from drill hole VNIIO-1988-Sht-01 on the shelf of the Barents Sea (Report 6404, Murmansk)

Interareal correlation has been carried out; composition of the deposits has been determined; sections recovered by marine drilling have been compared; reconstructed paleogeographic conditions confirm previous views on Jurassic and Cretaceous sedimentation in the area: 1. Determinate changes of continental and shallow marine mainly sandy Middle Jurassic deposits by sandy-clayey marine ones to the north and west occur. This indicates similar direction of clastic material migration and converse direction of Jurassic marine transgressions. 2. Increase of sand contents in the deposits also to the east and to the southeast indicates an important source of clastic material. It can result from incipience and development of the epiplatform orogen of Novaya Zemlya - Pai-Khoi in the Late Triassic - Early Jurassic. 3. Compositional and facial changes as well as changes in thicknesses of some Early Cretaceous lithologic-stratigraphic complexes indicate fast change of terrigenous material transport from the north to the south - south-east in the Late Valanginian - Hauterivian. Besides within the South Barents Sea region up to the Shtokman area there occurs weak variability in lithologic parameters of Neocomian avandeltaic deposits and turbidites composed of clays, claystones, and clayey siltstones. Correlation of drilling sections from the Shtokman area and from the South Basin of the Barents Sea together with paleotectonic analysis result to the conclusion about significant structure-forming movements in the Late Jurassic - Early Neocomian. During this time there occurred maximal growth of the Shtokman structure and likely of many other structures belonging to the South Basin of the Barents Sea.

Molecular origin of cancer: Catechol estrogen-3,4-quinones as endogenous tumor initiators

Cancer is a disease that begins with mutation of critical genes: oncogenes and tumor suppressor genes. Our research on carcinogenic aromatic hydrocarbons indicates that depurinating hydrocarbon–DNA adducts generate oncogenic mutations found in mouse skin papillomas (Proc. Natl. Acad. Sci. USA 92:10422, 1995). These mutations arise by mis-replication of unrepaired apurinic sites derived from the loss of depurinating adducts. This relationship led us to postulate that oxidation of the carcinogenic 4-hydroxy catechol estrogens (CE) of estrone (E1) and estradiol (E2) to catechol estrogen-3,4-quinones (CE-3, 4-Q) results in electrophilic intermediates that covalently bind to DNA to form depurinating adducts. The resultant apurinic sites in critical genes can generate mutations that may initiate various human cancers. The noncarcinogenic 2-hydroxy CE are oxidized to CE-2,3-Q and form only stable DNA adducts. As reported here, the CE-3,4-Q were bound to DNA in vitro to form the depurinating adduct 4-OHE1(E2)-1(α,β)-N7Gua at 59–213 μmol/mol DNA–phosphate whereas the level of stable adducts was 0.1 μmol/mol DNA–phosphate. In female Sprague–Dawley rats treated by intramammillary injection of E2-3,4-Q (200 nmol) at four mammary glands, the mammary tissue contained 2.3 μmol 4-OHE2-1(α,β)-N7Gua/molDNA–phosphate. When 4-OHE1(E2) were activated by horseradish peroxidase, lactoperoxidase, or cytochrome P450, 87–440 μmol of 4-OHE1(E2)-1(α, β)-N7Gua was formed. After treatment with 4-OHE2, rat mammary tissue contained 1.4 μmol of adduct/mol DNA–phosphate. In each case, the level of stable adducts was negligible. These results, complemented by other data, strongly support the hypothesis that CE-3,4-Q are endogenous tumor initiators.