十二週鋅補充對氣喘兒童肺功能、 氧化壓力與抗氧化能力之影響

氣喘為兒童常見之慢性呼吸道發炎性疾病，氧化壓力及抗氧化失衡在其病理機轉中扮演關鍵角色。鋅具有抗氧化與免疫調節功能，近年研究顯示其可能有助於改善氣喘相關症狀與肺功能表現。惟目前針對兒童氣喘患者進行鋅補充介入之臨床試驗仍有限。本研究探討十二週鋅補充對氣喘兒童肺功能、氧化壓力及抗氧化能力之影響。研究採隨機雙盲對照設計，共納入 51 名 6 至 16 歲氣喘兒童，隨機分派至補充劑組（每日 10 毫克鋅）與安慰劑組，進行 12 週介入。研究期間評估介入前後之肺功能、氧化壓力（GSSG/GSH 比值）及抗氧化能力 (SOD、GSH、GSSG) 及飲食攝取資料。結果顯示，兩組介入前皆無鋅缺乏狀態，補充劑組介入後血清鋅濃度有上升趨勢，安慰劑組則下降，但皆未達顯著差異。肺功能部份，補充劑組介入後 FeNO 濃度顯著改善，FeNO 變化量較安慰劑組顯著降低 (β = −13.43，p = 0.02)。有別於安慰劑組，鋅補充組雖同樣呈現 GSH 降低與 GSSG/GSH 比值上升，但其未觀察到 GSSG 顯著累積。且該組血清鋅濃度變化量與 SOD 活性變化量呈顯著正相關 （r = 0.54，p = 0.01）。 因此本研究證實給予氣喘兒童12 週鋅補充可顯著改善氣喘兒童 FeNO 濃度及中央氣道阻力，顯示氣喘兒童補充鋅可能有助減緩氣道發炎與重塑。然而，鋅是否透過 SOD 抗氧化機制影響肺功能，尚待進一步研究。未來可進一步增加樣本數與延長介入期，以確認其長期效益與臨床應用。

Asthma is the most common chronic inflammatory airway disorder among children, in which oxidative stress and impaired antioxidant defense mechanisms are recognized as key contributors to disease pathogenesis. Zinc, an essential trace element with established antioxidant and immunomodulatory functions, has been increasingly implicated in the modulation of airway inflammation and pulmonary function. Nevertheless, clinical evidence regarding zinc supplementation in pediatric asthma populations remains scarce. This randomized, double-blind, placebo-controlled trial aimed to investigate the effects of a 12-week zinc supplementation regimen on pulmonary function, oxidative stress, and antioxidant capacity in asthmatic children. A total of 51 participants aged 6 to 16 years with physician-diagnosed asthma were randomly allocated to receive either a daily zinc supplement (10 mg/day) or a placebo for 12 weeks. Outcome measures included spirometry, fractional exhaled nitric oxide (FeNO), oxidative stress biomarkers (GSSG/GSH ratio), antioxidant enzyme activity (SOD, GSH and GSSG), and dietary intake assessment. At baseline, none of the participants exhibited zinc deficiency. Post-intervention, the zinc group demonstrated a non-significant increase in serum zinc levels, whereas the placebo group exhibited a decreasing trend. Importantly, the zinc-supplemented group showed a statistically significant reduction in FeNO levels compared to placebo (β = −13.43，p = 0.02), indicative of attenuated airway inflammation. Although both groups experienced a decline in GSH and an elevation in the GSSG/GSH ratio, only the placebo group exhibited significant GSSG accumulation. Moreover, a positive correlation was observed between changes in serum zinc concentrations and SOD activity within the supplementation group （r = 0.54，p = 0.01）, suggesting a potential link between zinc status and antioxidant defense. These findings indicate that 12-week zinc supplementation may confer beneficial effects on airway inflammation and central airway resistance in pediatric asthma, potentially through modulation of antioxidant pathways. Further studies with larger sample sizes and prolonged follow-up are needed to clarify the mechanisms and validate the long-term therapeutic potential of zinc in in pediatric asthma.