Abstract
The aim of the current study was to examine the preventive effect of green tea catechins on the transport of Benzo[a]pyrene (B[α]P) into the brain using an in vitro bio-mimic system coupled with sequential co-cultures. When 72 μM of catechins was pre-treated, cellular cytotoxicity induced by IC50 of B[α]P in human liver hepatocellular carcinoma (HepG2) and human brain microvascular endothelial cells (HBMECs) was reduced by 27% and 26%, respectively. The cellular integrity measured in HBMECs, which was exposed to IC50 of B[α]P, slowly decreased. However, the pre-treatment of catechins retained cellular integrity that was 1.14 times higher than with the absence of catechins. Co-consumption of catechins reduced not only the bio-accessibility of B[α]P in digestive fluid, but it also decreased absorption of B[α]P in human intestinal epithelial cells (Caco-2) with a HepG2 co-culture system. It was found that approximately a two times lower amount of B[α]P was transported via the blood-brain barrier (BBB) compared to only the B[α]P intake. These results are taken in conjunction with each other support that catechins could be able to prevent brain toxicity induced by B[α]P in the human body by limiting the bio-availability of B[α]P.
Highlights
Polycyclic aromatic hydrocarbons (PAHs) are generally recognized as one of the environmental contaminants that significantly affect human carcinogenesis [1]
In order to evaluate the inhibitory effect of catechins on HepG2 cytotoxicity induced by B[α]P, various concentrations of catechins were pre-treated prior to incubation of inhibit cell growth by 50% (IC50) of B[α]P
The current study evaluated the effect of green tea catechins on the cytotoxicity of hepatocyte and the blood-brain barrier using HepG2 and human brain microvascular endothelial cells (HBMECs), respectively
Summary
Polycyclic aromatic hydrocarbons (PAHs) are generally recognized as one of the environmental contaminants that significantly affect human carcinogenesis [1]. Benzo[a]pyrene (B[α]P) is mainly produced from burning wood, cigarette smoking, car exhausts, and smoked or grilled food [2,3]. It is absorbed through the skin, respiration, and the intake of contaminated food [4]. According to a previous study, human exposure to B[α]P through food intake was about 0.125 μg per day [6]. Even though B[α]P has been identified as a carcinogenic compound even at a low exposure concentration, tolerable daily intake (TDI) has not been generally established [7]
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
