{'fraction_non_alphanumeric': 0.022714036109493303, 'fraction_numerical': 0.009900990099009901, 'mean_word_length': 5.157706093189964, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Monoamine oxidase and semicarbazide sensitive amine oxidase activities in normal and inflamed human dental pulp.

BACKGROUND
Human dental pulp contains monoamine oxidase (MAO) and semicarbazide sensitive amine oxidase (SSAO). In other tissues SSAO is involved in oxidative stress and inflammation, but the role of MAO and SSAO in human pulp and changes of their activities in reversible pulpitis still remains poorly understood.


MATERIAL/METHODS
We investigated MAO labeling with mechanism-based inhibitor [3H]pargyline activities of MAO A, MAO B, and SSAO in healthy and inflamed human dental pulp.


RESULTS
Incubation of human dental pulp homogenates with [3H]pargyline caused MAO labeling. MAO activity assayed with 100 microM [14C]5HT or 10 microM [14C]PEA was sensitive to selective inhibitors of MAO A and MAO B, respectively. MAO activity with 50 microM [14C]PEA was partially inhibited by clorgyline, and total inhibition was achieved only by the combination of clorgyline and semicarbazide, suggesting the presence of SSAO. Inflammation of the dental pulp was accompanied by a significant decrease in MAO labeling, MAO B (but not MAO A) activity and the increase in SSAO activity.


CONCLUSIONS
The results of the present study suggest that the increase of dental pulp SSAO activity contributes to the development of inflammation in the dental pulp. The decrease in MAO B activity and lack of significant changes in MAO A activity may be associated with an anti-inflammatory response - inflamed pulp MAO A still effectively deaminates the inflammatory mediator 5HT, whereas inhibition of MAO B could result in some decrease of hydrogen peroxide generation, essential for the tissue damage in inflammation.