DiSilvestro R A, Carlson G P
Ohio State University, Columbus 43210.
Free Radic Biol Med. 1994 Jan;16(1):57-61. doi: 10.1016/0891-5849(94)90243-7.
Low zinc (Zn) intake could be expected to compromise resistance to oxidative stress, even when accompanied by a normally protective acute phase response pretreatment. Mildly Zn deficient rats showed very high degrees of CCl4-induced hepatic cell membrane injury as assessed by serum sorbitol dehydrogenase activities. Rats pair-fed adequate Zn also showed above normal degrees of injury, but much less than rats fed low Zn. An acute phase response, elicited by leg inflammation, strongly protected rats consuming adequate Zn, either ad libitum or pair-fed, against the CCl4-induced rise in sorbitol dehydrogenase. However, the effect was partially absent in rats fed low Zn. Zinc intake had no effect on CCl4-produced microsomal injury, assessed by glucose-6-phosphatase activities. Rats fed low Zn showed normal hepatic levels of metallothionein, a Zn protein with proposed antioxidant functions, but did not show the rise in metallothionein levels normally associated with acute phase response. In summary, mild Zn deficiency caused poor resistance to CCl4-induced plasma membrane injury and partially negated acute phase response protective effects. Metallothionein was not involved in the former effect, but may have contributed to the latter.
即使伴有通常具有保护作用的急性期反应预处理，低锌（Zn）摄入仍可能会损害对氧化应激的抵抗力。通过血清山梨醇脱氢酶活性评估，轻度缺锌大鼠表现出非常高程度的四氯化碳诱导的肝细胞膜损伤。配对喂养充足锌的大鼠也表现出高于正常程度的损伤，但远低于低锌喂养的大鼠。腿部炎症引发的急性期反应能强烈保护自由采食或配对喂养充足锌的大鼠，使其免受四氯化碳诱导的山梨醇脱氢酶升高的影响。然而，低锌喂养的大鼠这种保护作用部分缺失。通过葡萄糖-6-磷酸酶活性评估，锌摄入量对四氯化碳产生的微粒体损伤没有影响。低锌喂养的大鼠肝组织中金属硫蛋白水平正常，金属硫蛋白是一种具有抗氧化功能的锌蛋白，但并未表现出通常与急性期反应相关的金属硫蛋白水平升高。总之，轻度缺锌导致对四氯化碳诱导的质膜损伤抵抗力差，并部分抵消了急性期反应的保护作用。金属硫蛋白不参与前者的作用，但可能对后者有贡献。
