Quote from Dr. Garrett Smith on January 1, 2019, 4:02 pm

This is pretty significant.  In mice that were genetically unable to store Poison/"Vitamin A" in their livers, the researchers were UNABLE to induce toxicity in their livers with thioacetamide (known hepatotoxin).  Once they gave those mice Poison/"Vitamin A" though, their livers quickly showed all the normal damage that was expected.  How many liver problems today would be avoided if so many people weren't Poison/"Vitamin A" toxic?  Who knows...

Retinoids Modulate Thioacetamide-Induced Acute Hepatotoxicity

The literature indicates that retinoids can influence the metabolism and actions of xenobiotics and conversely that xenobiotics can influence the metabolism and actions of retinoids. We were interested in understanding the degree to which hepatic retinoid stores, accumulated over a lifetime, affect xenobiotic metabolism, and actions. To investigate this, we induced liver injury through administration of the hepatotoxin thioacetamide (TAA) to chow fed wild type (WT) mice and lecithin:retinol acyltransferase-deficient (Lrat^−/−) mice that are genetically unable to accumulate hepatic retinoid stores. Within 48 h of TAA-treatment, WT mice develop liver injury as evidenced by focal necrotic areas and increases in serum ALT activity and myeloperoxidase activity in hepatic parenchyma. Simultaneously, features of hepatic encephalopathy develop, as evidenced by a 25% increase in blood ammonia and a threefold reduction of blood glucose levels. This is accompanied by reduced hepatic glutathione, and increased thiobarbituric acid reactive substances, protein carbonyl and sulfhydryl groups, and increased cytochrome P450-catalyzed hydroxylation activity and flavin-containing monooxygenase activity in microsomes prepared from WT liver. Strikingly, none of these TAA-induced effects were observed for matched Lrat^−/− mice.

The wild-type mice that could store Poison/"Vitamin A" in their livers got thoroughly messed up (technical term) from the thioacetamide.

The Lrat-/- mice that are genetically unable to store Poison/"Vitamin A" in their livers had NO PROBLEMS from the thioacetamide.

So...is it the thioacetamide that is the toxin, or is it the Poison/"Vitamin A"?  Keep reading.

To confirm that TAA hepatotoxicity depends on retinoid availability, we administered, over 48 h, four oral doses of 3000 IU retinyl acetate each to the mice. This led to the development of hepatotoxicity in Lrat^−/− mice that was similar in extent to that observed in WT mice. Our findings establish that endogenous hepatic retinoid stores can modulate the toxicity of TAA in mice.

Once the Lrat-/- mice (the ones who couldn't store Poison/"Vitamin A" in their livers and didn't get poisoned) were GIVEN VITAMIN A, then they got toxicity from the thioacetamide just like the "normal" wild-type mice.

It is not the thioacetamide that is the star toxin here, folks.  I hope you can see this.  The key ingredient is the Poison/"Vitamin A".