Methylcholanthrene is often tested on mice and rats to derive information for cancer medicine development.
It is also known that due to genetic mutations, the compound causes cancer cells to develop.
At -60 ̊C the reaction of 1 and 2 afforded evenly to the lactone (3), the carbonyl addition product which underwent conversion on treatment with acid.
Cyclization of the product occurred when treated with ZnCl2 in acetic acid anhydride and gave the compound 6-acetoxy-3-MC (5).
Unpublished observations of Venkatesan, Argus and Arcos suggest that demethylase synthesis inhibition is most plausible.
It is hard to determine how when the equilibrium is formed due to difficulties with radioactive measurements.
[11] MC is metabolized by rat liver microsomes into oxygenated forms which alkylate DNA.
In a study from 1991, lung precancerous and cancerous lesions were induced in Wistar rats by one intrabronchial injection of 3-MC.
[13] Jin et al. (2013) found that the cellular redox balance is altered by acute exposure to 3-MC.
[14] 3-MC is a ligand of the aryl hydrocarbon receptor (AhR), which stimulates transcription directed by xenobiotic response elements.
3-MC was found to elicit estrogenic activity by this mechanism, and by stimulation of the expression of some endogenous ER target genes.
Curren et al. (1978) were the first to report successfully induced mutations in human cells with 3-MC.
Skin epithelial cells are thought to metabolize the compound to mutagenic products.
[17] The ability to metabolize mutagens may express genetically regulated differences within a species such as man or mouse, causing environmental chemicals to show a different level of mutagenicity and carcinogenicity to specific individuals.
Miller et al. (1990) compared the effects of fetal versus adult exposure to 3-MC on both induction of aryl hydrocarbon hydroxylase (AHH) activity in lung and dependence of lung tumorigenesis on the Ah genotype.
The same injections to adult F1 mice revealed only a 4- to 7—fold increase in lung AHH activity, compared to the large fetal induction ratio.