Abstract
We had previously shown that the intake of scallop mantle tissue resulted in the death of mice and rats. In this study, we investigated the liver injury caused by mantle tissue to clarify the mechanism behind its toxicity. Mantle toxin increased lipid peroxidation and decreased the reductive thiol content as well as the DPPH radical scavenging activity, catalase activity, and glutathione content in the liver of the mice. These results suggested that the mantle tissue diet caused oxidative stress through the decrease in antioxidants. In addition, mantle toxin increased the mRNA expression of endoplasmic reticulum (ER) stress‐ and inflammation‐induced genes and the protein expression of caspase‐3 and Bax (which induce apoptosis), suggesting that the mantle tissue diet causes apoptosis through oxidative stress, ER stress, and inflammation in the liver tissue. Such liver injury may be an essential cause of the rodent demise.
Highlights
We investigated several indicators of liver injury in mice fed a diet of toxic mantle tissue in order to clarify the
Significant differences were not found (Figure 2). These results show that the mantle diet causes oxidative stress by decreasing the antioxidants in the liver tissue
We investigated the of insulin receptor substrate in the liver tissue, resulting in the inhi
Summary
Divided randomly into two groups (5 or 6 mice per group) and causing toxins in the liver after oral administration. One study found fed a diet without (control diet) or with 3% mantle tissue including that oral treatment with yessotoxin (a toxin that causes epithelial cell layer (mantle diet) for 4–8 weeks. The mice were fed 4 g of each diet every the liver enzymes aspartate aminotransferase (AST) and alanine day, and the amount of food consumption was measured daily as aminotransferase (ALT), which typically increase in hepatic injury, an index of toxicity (Hasegawa et al, 2018). We investigated several indicators of liver injury in mice fed a diet of toxic mantle tissue in order to clarify the.
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.
