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home > glutathione and tamoxifen induced hepatotoxicity via gut microbiota-mediated hyodeoxycholic acid depletion Farnesoid X receptor signaling disruption: Gut Microbes: Vol 18, No 1 Availiable in:50ml > glutathione and tamoxifen induced hepatotoxicity via gut microbiota-mediated hyodeoxycholic acid depletion Farnesoid X receptor signaling disruption: Gut Microbes: Vol 18, No 1 Availiable in:50ml
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glutathione and tamoxifen induced hepatotoxicity via gut microbiota-mediated hyodeoxycholic acid depletion Farnesoid X receptor signaling disruption: Gut Microbes: Vol 18, No 1 Availiable in:50ml
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glutathione and tamoxifen induced hepatotoxicity via gut microbiota-mediated hyodeoxycholic acid depletion Farnesoid X receptor signaling disruption: Gut Microbes: Vol 18, No 1 Availiable in:50ml

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Although excessive or uncontrolled frying can favor the formation of compounds with toxicological potential, such as acrylamide, polycyclic aromatic hydrocarbons and advanced glycation end products, common commercial practices generally maintain their levels within limits considered safe, and recent data show that acrylamide reaches maximum concentrations in the early stages of frying and subsequently decreases through thermal degradation, while antioxidant activity is relatively preserved due to the concomitant formation of new bioactive compounds, supporting the current concept according to which the frying process simultaneously generates both potentially harmful molecules and molecules with a protective effect, the final proportion available for physiological activity being further influenced by the preparation method and extraction parameters [49,50,51,52,53]

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glutathione and tamoxifen induced hepatotoxicity via gut microbiota-mediated hyodeoxycholic acid depletion Farnesoid X receptor signaling disruption: Gut Microbes: Vol 18, No 1 Availiable in:50ml

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