Harris S S, Navia J M
J Nutr. 1978 Nov;108(11):1777-82. doi: 10.1093/jn/108.11.1777.
The metabolism of sulfated glycosaminoglycans (GAG) in bone has been found to be altered in vitamin A deficiency. A neonatal rat calvarium model system was used to determine if these changes are related to catabolic defects. Two day old rat pup calvaria were cultured in media containing serum from A- or A+ rats and radiolabeled sulfate or glucosamine. The incorporation of 35S-sulfate into the GAG fraction of calvaria cultured with A- serum for 48 hours was significantly increased compared to the values found in calvaria cultured with A+ serum (A-, 1,970 +/- 300; A+, 940 +/- 177; X +/- SD). The uptake of 35S-sulfate into the GAG fraction of calvaria cultured with A- serum showed continuous increase over 96 hours,whereas, 35S-sulfate uptake leveled off after 24 hours in the A+ group. There was also a significant increase in [14C]glucosamine uptake into the GAG fractions of calvaria cultured with A-serum (A-, 1,966 +/- 537; A+, 1,662 +/- 244; X +/- SD). To determine if the alteration in metabolism of sulfated GAG was in the biosynthetic or degradative pathways, a chase study was performed in which the calvaria were prelabeled with 35SO4. The rate of tissue loss of 35S-sulfate was lower in the total digests and the GAG fractions from calvaria cultured with A- serum than those cultured with A+ serum. Thus, the alteration in the metabolism of the sulfated GAG resulting from A- culture conditions seems to be defect in the degradative process.
研究发现，维生素A缺乏会改变骨骼中硫酸化糖胺聚糖（GAG）的代谢。采用新生大鼠颅骨模型系统来确定这些变化是否与分解代谢缺陷有关。将两天大的大鼠幼崽颅骨在含有来自维生素A缺乏（A-）或维生素A充足（A+）大鼠血清的培养基中培养，并加入放射性标记的硫酸盐或葡萄糖胺。与用A+血清培养的颅骨相比，用A-血清培养48小时的颅骨中，35S-硫酸盐掺入GAG部分的量显著增加（A-组为1970±300；A+组为940±177；均值±标准差）。用A-血清培养的颅骨中，35S-硫酸盐掺入GAG部分的量在96小时内持续增加，而在A+组中，35S-硫酸盐的摄取在24小时后趋于平稳。用A-血清培养的颅骨中，[14C]葡萄糖胺摄取到GAG部分的量也显著增加（A-组为1966±537；A+组为1662±244；均值±标准差）。为了确定硫酸化GAG代谢的改变是发生在生物合成途径还是降解途径，进行了一项追踪研究，其中颅骨先用35SO4进行预标记。用A-血清培养的颅骨总消化物和GAG部分中，35S-硫酸盐的组织损失率低于用A+血清培养的颅骨。因此，A-培养条件导致的硫酸化GAG代谢改变似乎是降解过程中的缺陷。
