Short-term adolescent nicotine exposure in rats elicits immediate and delayed deficits in T-lymphocyte function: critical periods, patterns of exposure, dose thresholds.
Short-term adolescent nicotine exposure in rats elicits immediate and delayed deficits in T-lymphocyte function: critical periods, patterns of exposure, dose thresholds.
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大鼠短期青少年尼古丁暴露会引起 T 淋巴细胞功能的立即和延迟缺陷：关键时期、暴露模式、剂量阈值。
DOI：
10.1080/14622200310001614610
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发表时间：
2003
期刊：
影响因子：
--
通讯作者：
Slotkin,TheodoreA
中科院分区：
文献类型：
--
作者：
Navarro,HernanA;Basta,PatriciaV;Seidler,FredericJ;Slotkin,TheodoreA
产前尼古丁暴露会导致T淋巴细胞有丝分裂的持续缺陷，并且脆弱期会延伸到青春期，这是通常开始吸烟的阶段。我们探讨了尼古丁暴露模式（连续输注与重复皮下注射）、剂量-效应关系和效应特异性的重要性。从出生后第30天（PN）开始，使用产生与吸烟者相似的血浆尼古丁水平（25 ng/ml）的方案（6 mg/kg/天）对青春期大鼠进行尼古丁输注1周;另一组接受2 mg/kg/天。输注期结束时（PN 37），6 mg/kg/天剂量组伴刀豆球蛋白A的T淋巴细胞促有丝分裂反应不足; 2 mg/kg/天剂量组的数值介于对照组和6 mg/kg/天剂量组之间。尼古丁治疗终止后一周，反应恢复正常，仅在成年早期（PN 65）再次出现，在该阶段，即使对于接受2 mg/kg/天剂量的组，不良反应也很显著。与T细胞改变相反，B淋巴细胞反应不受影响。在1周治疗期内通过每日两次皮下注射给予相同总剂量的尼古丁（每次注射1或3 mg/kg），未引起T细胞或B细胞反应缺陷，即使高剂量产生明显的全身毒性和持续性体重减轻。我们的研究结果表明，青少年尼古丁暴露，即使在低于主动吸烟，激发T淋巴细胞功能的选择性缺陷。虽然短期的适应可能会纠正这种影响，但尽管停止尼古丁暴露，在年轻的成年期，赤字会再次出现。
Prenatal nicotine exposure elicits lasting deficiencies in T-lymphocyte mitogenesis, and the period of vulnerability extends into adolescence, the stage at which smoking typically commences. We explored the importance of nicotine exposure patterns (continuous infusion vs. repeated subcutaneous injections), dose–effect relationships, and specificity of the effects. Adolescent rats were given nicotine infusions for 1 week beginning on postnatal day (PN) 30, using a regimen (6 mg/kg/day) that produces plasma nicotine levels (25 ng/ml) similar to those in smokers; another group received 2 mg/kg/day. At the end of the infusion period (PN37), T-lymphocyte mitogenic responses to concanavalin A were deficient in the group receiving 6 mg/kg/day; values for the 2 mg/kg/day group were intermediate between controls and the 6 mg/kg/day group. One week after the termination of nicotine treatment, responses returned to normal, only to reemerge in young adulthood (PN65), at which stage adverse effects were significant even for the group that received 2 mg/kg/day. In contrast to the T-cell alterations, B-lymphocyte responses were unaffected. Administering the same total doses of nicotine by twice-daily subcutaneous injections over the 1-week treatment period (1 or 3 mg/kg per injection) did not evoke deficits in responses of either T-cells or B-cells, even though the high dose produced overt systemic toxicity and persistent weight loss. Our results indicate that adolescent nicotine exposure, even at levels below those associated with active smoking, elicits selective deficits in T-lymphocyte function. Although short-term adaptations may correct the effects, deficits reemerge in young adulthood despite cessation of nicotine exposure.
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