You got that wrong. It is not that nicotine induces masculine features; it's that manly men like to smoke! It's true: guys with high natural levels of testosterone then to have a stronger dopaminergic activity in their nucleus accumbens, which in turn triggers the desire to smoke - and consume psychostimulants. Hope this helps! 
SUCKMYMUSCLE
I agree with what you say but just to confirm anti-estrogen effects of nicotine:
Tobacco alkaloid derivatives as inhibitors of breast cancer aromatase.
Kadohama N, Shintani K, Osawa Y.
Endocrine Biochemistry Department, Medical Foundation of Buffalo Research Institute, N.Y. 14203.
The inhibition of estrogen biosynthesis by the use of aromatase inhibitors is emerging as a valuable approach to breast cancer therapy. Because smoking has a profound effect on estrogen-related processes we examined the ability of tobacco constituents to suppress estrogen production by breast cancer aromatase. N-n-octanoylnornicotine and N-(4-hydroxyundecanoyl) anabasine suppressed aromatase activity in culture of two human breast cancer cell lines, MDA-MB-231 (IC50 of 310 and 20 microM, respectively) and SK-BR-3 (IC50 of 450 and approximately 2 microM, respectively). MDA-MB-231 cells induced by 250 nM dexamethasone or 1 mM (Bt)2cAMP were slightly more sensitive to both inhibitors. Kinetic analyses showed that inhibition by N-(4-hydroxyundecanoyl)anabasine is competitive with respect to androstenedione as substrate, with apparent Ki values of 0.2 microM against microsomal aromatase activity derived from both (Bt)2cAMP-induced MDA-MB-231 cells and human breast tumor tissue. The corresponding apparent Ki against human placental microsomal aromatase activity was 0.4 microM.
These results indicate that acyl derivatives of nornicotine and anabasine block estrogen formation in breast tumor cells and tissue and could contribute to the decreased intra-tissue estrogen levels in women who smoke.PMID: 8313352 [PubMed - indexed for MEDLINE]
1: Endocr Res. 1991;17(3-4):409-19.Related Articles, Links
Competitive inhibition of human placental aromatase by N-n-octanoylnornicotine and other nornicotine derivatives.
Bullion K, Ohnishi S, Osawa Y.
Endocrine Biochemistry Department, Medical Foundation of Buffalo Research Institute, NY 14203.
In a study of the effect of N-n-octanoylnornicotine and other acyl derivatives of nornicotine on the aromatization of androstenedione by human placental microsomal aromatase, we found that N-n-octanoylnornicotine, a component of cigarette smoke, exhibited competitive inhibition with an apparent Ki of 0.65 microM. This is comparable to that of aminoglutethimide, the clinically-used non-steroidal aromatase inhibitor. N-n-Decanoylnornicotine and N-(4-hydroxyundecanoyl)nornicotine exhibited apparent Ki values of 0.86 microM and 0.24 microM, respectively.
This study suggests that cigarette smoke components may have a direct effect on estrogen biosynthesis and that these compounds may prove to be useful parent structures for development of active site probes for further elucidation of estrogen biosynthesis and might eventually lead to the development of alternative non-steroidal anti-cancer therapy.PMID: 1811989 [PubMed - indexed for MEDLINE]
Nicotine and estrogen metabolism--possible implications of smoking for growth and outcome of treatment of hormone-dependent cancer? Discussion of experimental results.
Zeller WJ, Berger MR.
Institute of Toxicology and Chemotherapy, German Cancer Research Center, Heidelberg.
The combination treatment of hormone-dependent autochthonous mammary carcinomas in the rat with nicotine plus HECNU, a water-soluble nitrosourea, resulted in a potentiation of antitumor action. Nicotine and its metabolite cotinine are strong inhibitors of the aromatase.
With regard to investigations in smoking women, suggesting a decreased endogenous estrogen production, our results indicate that smoking might influence growth and treatment results of hormone-dependent human cancer.PMID: 2606936 [PubMed - indexed for MEDLINE]
Fertil Steril. 1986 Aug;46(2):232-6.Related Articles, Links
Constituents of cigarette smoke inhibit human granulosa cell aromatase.
Barbieri RL, McShane PM, Ryan KJ.
Recent epidemiologic studies suggest that women smokers have lower endogenous estrogen levels than nonsmokers. The effects of aqueous extracts of cigarette smoke on aromatase were evaluated in cultures of human granulosa cells. Aqueous extracts of cigarette smoke inhibited the conversion of androstenedione (delta 4A) to estradiol in a dose-dependent manner. Dialysis experiments demonstrated that 90% of the inhibitory activity of aqueous extracts of cigarette smoke was in the less than 1000 mol wt fraction. Removal of the aqueous extract of cigarette smoke from the culture medium resulted in a complete reversal of the inhibition of delta 4A aromatization. Addition of supraphysiologic concentrations of delta 4A (73 microM) to the culture medium blocked the smoke-induced inhibition of aromatization. Two low-molecular-weight components of cigarette smoke, nicotine and anabasine, inhibited granulosa cell aromatase in a dose-dependent manner. These studies suggest that constituents of cigarette smoke inhibit a major steroidogenic pathway.
J Clin Invest. 1986 Jun;77(6):1727-33.Related Articles, Links IPB Image
Nicotine, cotinine, and anabasine inhibit aromatase in human trophoblast in vitro.
Barbieri RL, Gochberg J, Ryan KJ.
Epidemiologic studies suggest that women who smoke have lower endogenous estrogen than nonsmokers. To explore the possible link between cigarette smoking and decreased endogenous estrogens, we have examined the effects of constituents of tobacco on estrogen production in human choriocarcinoma cells and term placental microsomes. In choriocarcinoma cell cultures, nicotine, cotinine (a major metabolite of nicotine), and anabasine (a minor component of cigarette tobacco) all inhibited androstenedione conversion to estrogen in a dose-dependent fashion. Removal of nicotine, cotinine, and anabasine from the culture medium resulted in the complete reversal of the inhibition of aromatase. In the choriocarcinoma cell cultures, a supraphysiologic concentration of androstenedione (73 microM) in the culture medium blocked the inhibition of aromatase caused by nicotine, cotinine, and anabasine. In preparations of term placental microsomes, nicotine, cotinine, and anabasine inhibited the conversion of testosterone to estrogen. Kinetic analysis demonstrated the inhibition to be competitive with respect to the substrate.
These findings suggest that some nicotinic alkaloids directly inhibit aromatase. This mechanism may explain, in part, the decreased estrogen observed in women who smoke.
PMID: 3711333 [PubMed - indexed for MEDLINE
