Alfos S, Higueret P, Pallet V, Higueret D, Garcin H, Jaffard R
Laboratoire de Nutrition, Université Bordeaux I, Talence, France.
Neurosci Lett. 1996 Mar 15;206(2-3):73-6. doi: 10.1016/s0304-3940(96)12455-1.
It is known that alcohol induces disorders in the metabolism of retinoids and particularly in the biosynthetic pathways of retinoic acid (RA). Since RA has, along with other hormones and particularly triiodothyronine (T3), a physiological role in the adult brain, the effect of chronic exposure to alcohol on RA and T3 status was investigated. The amounts of RA receptor (RAR) and T3 receptor (TR) mRNAs were quantified and the activity of the 'tissue' transglutaminase (tTG; an RA-dependent enzyme) was assayed in the brain of mice following chronic ethanol consumption (CEC; 12% v/v for 6-10 months). Compared to controls, ethanol-treated mice exhibited increased amounts of RAR and TR mRNAs together with an increase in tTG activity. It is hypothesized that the enhanced cellular action of RA and T3 could play a role in the previously described brain damages induced by CEC.
众所周知，酒精会导致类视黄醇代谢紊乱，尤其是在维甲酸（RA）的生物合成途径中。由于RA与其他激素，特别是三碘甲状腺原氨酸（T3）一样，在成人大脑中具有生理作用，因此研究了长期接触酒精对RA和T3状态的影响。在慢性乙醇摄入（CEC；12% v/v，持续6 - 10个月）后的小鼠大脑中，对RA受体（RAR）和T3受体（TR）mRNA的量进行了定量，并测定了“组织”转谷氨酰胺酶（tTG；一种RA依赖性酶）的活性。与对照组相比，乙醇处理的小鼠表现出RAR和TR mRNA量的增加以及tTG活性的增加。据推测，RA和T3增强的细胞作用可能在先前描述的由CEC引起的脑损伤中起作用。
