Assessment of In Vitro Bioaccessibility and In Vivo Oral Bioavailability as Complementary Tools to Better Understand the Effect of Cooking on Methylmercury, Arsenic, and Selenium in Tuna

Fish consumption is the main exposure pathway of the neurotoxicant methylmercury (MeHg) in humans. The risk associated with exposure to MeHg may be modified by its interactions with selenium (Se) and arsenic (As). In vitro bioaccessibility studies have demonstrated that cooking the fish muscle decreases MeHg solubility markedly and, as a consequence, its potential absorption by the consumer. However, this phenomenon has yet to be validated by in vivo models. Our study aimed to test whether MeHg bioaccessibility can be used as a surrogate to assess the effect of cooking on MeHg in vivo availability. We fed pigs raw and cooked tuna meals and collected blood samples from catheters in the portal vein and carotid artery at: 0, 30, 60, 90, 120, 180, 240, 300, 360, 420, 480 and 540 min post-meal. In contrast to in vitro models, pig oral bioavailability of MeHg was not affected by cooking, although the MeHg kinetics of absorption was faster for the cooked meal than for the raw meal. We conclude that bioaccessibility should not be readily used as a direct surrogate for in vivo studies and that, in contrast with the in vitro results, the cooking of fish muscle did not decrease the exposure of the consumer to MeHg.

Automated summary

This study found that although in vitro models showed that cooking fish muscle can significantly decrease the bioaccessibility of MeHg, it did not have the same effect in in vivo experiments. The research suggests that bioaccessibility is not suitable as a direct surrogate for evaluating the effect of cooking on MeHg availability in the body.