Self- Perceived Stress in Relation to Anxiety, Depression and Health-related Quality of Life among Health Professions Students: A Cross-sectional Study from Bosnia and Herzegovina.

Introduction: The purpose of the present study was to examine self-perceived stress of health professions students at the Faculty of Medicine Foča, and to explore its association with anxiety, depression and health-related quality of life.

Methods: The cross-sectional study enrolled 451 students at the Faculty of Medicine (medicine, dentistry, nursing and speech therapy). Survey instruments were distributed at the conclusion of the spring semester during the last required lecture for each year and study programme class.

Identification and quantification of stable DNA adducts formed from dibenzo[a,l]pyrene or its metabolites in vitro and in mouse skin and rat mammary gland.

The stable adducts of dibenzo[a,l]pyrene (DB[a,l]P) formed by rat liver microsomes in vitro were previously quantified, whereas the depurinating adducts were both identified and quantified [Li, et al. (1995) Biochemistry 34, 8043]. In this article, we report the identification and quantification of the stable DNA adducts obtained from DB[a,l]P and DB[a,l]P-11,12-dihydrodiol activated by rat liver microsomes and from reaction of (+/-)-anti-DB[a,l]P-11,12-dihydrodiol-13,14-epoxide (DB[a,l]PDE) and (+/-)-syn-DB[a,l]PDE with DNA in vitro.

Identification and quantification of the depurinating DNA adducts formed in mouse skin treated with dibenzo[a,l]pyrene (DB[a,l]P) or its metabolites and in rat mammary gland treated with DB[a,l]P.

Dibenzo[a,l]pyrene (DB[a,l]P) is the most potent carcinogenic polycyclic aromatic hydrocarbon and has been identified in the environment. Comparative tumorigenicity studies in mouse skin and rat mammary gland indicate that DB[a,l]P is slightly more potent than DB[a,l]P-11,12-dihydrodiol and much more potent than (+/-)-syn-DB[a,l]P-11,12-dihydrodiol-13,14-epoxide {(+/-)-syn-DB[a,l]PDE} and (+/-)-anti-DB[a,l]PDE. We report here the identification and quantification of the depurinating adducts formed in mouse skin treated with DB[a,l]P, DB[a,l]P-11,12-dihydrodiol, (+/-)-syn-DB[a,l]PDE, or (+/-)-anti-DB[a,l]PDE and rat mammary gland treated with DB[a,l]P.

Genotoxic metabolites of estradiol in breast: potential mechanism of estradiol induced carcinogenesis.

Long term exposure to estradiol increases the risk of breast cancer in a variety of animal species, as well as in women. The mechanisms responsible for this effect have not been firmly established. The prevailing theory proposes that estrogens increase the rate of cell proliferation by stimulating estrogen receptor-mediated transcription and thereby the number of errors occurring during DNA replication.

Metabolism and DNA binding studies of 4-hydroxyestradiol and estradiol-3,4-quinone in vitro and in female ACI rat mammary gland in vivo.

Studies of estrogen metabolism, formation of DNA adducts, carcinogenicity, cell transformation and mutagenicity have led to the hypothesis that reaction of certain estrogen metabolites, predominantly catechol estrogen-3,4-quinones, with DNA can generate the critical mutations initiating breast, prostate and other cancers. The endogenous estrogens estrone (E1) and estradiol (E2) are oxidized to catechol estrogens (CE), 2- and 4-hydroxylated estrogens, which can be further oxidized to CE quinones. To determine possible DNA adducts of E1(E2)-3,4-quinones [E1(E2)-3,4-Q], we reported previously that the reaction of E1(E2)-3,4-Q with dG produces the depurinating adduct 4-hydroxyE1(E2)-1-N7Gua [4-OHE1(E2)-1-N7Gua] by 1,4-Michael addition (Stack et al.