Guzelian P S, O'Connor L, Fernandez S, Chan W, Giampietro P, Desnick R
Life Sci. 1982 Sep 13;31(11):1111-6. doi: 10.1016/0024-3205(82)90084-4.
Nonproliferating cultures of adult rat hepatocytes were found to lose 60-70% of cell-associated zinc during their first 24 h of incubation in standard, serum-free medium. The loss of zinc was accompanied by a profound loss (greater than 95%) in the activity of the zinc metalloenzyme, delta-aminolevulinic acid dehydratase, as well as a loss (greater than 85%) in the cellular content of immunoreactive delta-aminolevulinic acid dehydratase protein. Restoration of cellular zinc content by the addition of zinc to the culture medium partially prevented the losses of both delta-aminolevulinic acid dehydratase activity and immunoreactive protein. Since the spontaneous, selective loss of cellular zinc appears to have specific effects on a relevant hepatic function, this culture system constitutes a novel in vitro model of zinc deficiency in mature liver.
在标准无血清培养基中孵育的成年大鼠肝细胞非增殖培养物，在孵育的最初24小时内，细胞相关锌损失了60%-70%。锌的损失伴随着锌金属酶δ-氨基乙酰丙酸脱水酶活性的显著损失（超过95%），以及免疫反应性δ-氨基乙酰丙酸脱水酶蛋白细胞含量的损失（超过85%）。通过向培养基中添加锌来恢复细胞锌含量，部分地防止了δ-氨基乙酰丙酸脱水酶活性和免疫反应性蛋白的损失。由于细胞锌的自发、选择性损失似乎对相关肝功能有特定影响，因此该培养系统构成了成熟肝脏锌缺乏的新型体外模型。
