Abstract
We evaluated the possible protective effects of six polyphenols on benzo(a)pyrene (BaP)-induced cytotoxicity in Caco-2 cells. We show that treatment with quinic acid, ferulic acid, homovanillic acid, trolox and BaP decreased cell viability, whereas naringenin and eriodictyol affected viability in a bi-phasic manner with low concentrations decreasing viability whereas higher concentrations increase viability. Co-treatment with 20 μM eriodictyol or naringenin reduced BaP-induced cytotoxicity, including cell apoptosis, cell cycle progression, and oxidative stress. Our results show that the protective effect of eriodictyol was superior to that of naringenin. The potential protective mechanisms of eriodictyol on BaP-induced toxicity were investigated by proteomics. We identified 80 differentially expressed proteins (DEPs) with proteins associated with genetic information processing pathway representing the highest proportion and number of proteins responding to eriodictyol treatment, including key proteins such as RPA2, SNRPA, RAD23B, NUP155 and AARS. Our results provide new knowledge on how polyphenols may prevent BaP-induced carcinogenesis.
Highlights
Benzo(a)pyrene (BaP), a well-known genotoxic polycyclic aromatic hydrocarbon (PAH), is a ubiquitous environmental chemical carcinogen, mainly present in cigarette smoke, incompletely combusted crude oils, coal tars, and certain types of processed foods
We evaluated whether polyphenols are critical for reducing BaPinduced cell damage
Our results showed that RPA2 was up-regulated in the eriodictyol and BaP (E+B)/C group, with no significant change in the B/C group, indicating that eriodictyol prevents BaP-induced cytotoxicity by activating the expression of RPA2 to repair damaged DNA
Summary
Benzo(a)pyrene (BaP), a well-known genotoxic polycyclic aromatic hydrocarbon (PAH), is a ubiquitous environmental chemical carcinogen, mainly present in cigarette smoke, incompletely combusted crude oils, coal tars, and certain types of processed foods. Humans are exposed to BaP by inhalation and intake, via food which contributes with 97% of the intake. Long-term exposure to BaP can elicit genotoxic, neurotoxic, mutagenic and carcinogenic responses in various organs and tissues [1]. As part of its carcinogenic mechanism, BaP is activated by phase I and II metabolizing enzymes generating 7, 8-diol-9, 10-epoxide (BPDE), which may interfere with cellular processes by covalently binding to DNA, eventually linked to carcinogenesis [2]. BaP is associated with formation of reactive oxygen species (ROS) that may induce the generation of the highly reactive genotoxic BaP-quinone component, 8-hydroxy-2-deoxyguanosine, 8-oxo-dG [3]
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