酒精使用障碍对细胞衰老的影响。
Effect of alcohol use disorder on cellular aging.
机构信息
National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, MD, 20892, USA.
Laboratório de Genética Animal e Humana, Departamento de Biologia Geral, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Belo Horizonte, Brazil.
出版信息
Psychopharmacology (Berl). 2019 Nov;236(11):3245-3255. doi: 10.1007/s00213-019-05281-5. Epub 2019 Jun 3.
RATIONALE
Human telomeres consist of tandem repeats at chromosome ends which protect chromosomal DNA from degradation. Telomere shortening occurs as part of natural aging; however, life stressors, smoking, drug use, BMI, and psychiatric disorders could disrupt cell aging and affect telomere length (TL). In this context, studies have evaluated the effects of alcohol consumption on TL; however, results have been inconsistent, which may reflect diverse drinking cut-offs and categorizations.
OBJECTIVES
To help clarify this, the present study addresses the association of TL with alcohol use disorder (AUD), drinking behaviors, lifetime stress, and chronological age.
METHODS
TL was quantified as the telomere to albumin ratio (T/S ratio) obtained from peripheral blood DNA using the quantitative PCR assay, from 260 participants with AUD and 449 non-dependent healthy controls (HC) from an existing National Institute on Alcohol Abuse and Alcoholism (NIAAA) database.
RESULTS
AUD participants showed shorter TL compared to HC with both, age, and AUD, as independent predictors as well as a significant AUD with age interaction effect on TL. TL was also associated with impulsiveness in AUD participants. We did not observe an association between TL and chronicity of alcohol use, alcohol doses ingested, or childhood trauma exposures in either AUD or HC, although very few HC reported a history of childhood trauma.
CONCLUSION
Our results support previous findings of telomere shortening with chronic alcohol exposures and show both an effect of AUD on TL that is independent of age as well as a significant AUD by age interaction on TL. These findings are consistent with accelerated cellular aging in AUD.
背景
人类端粒由染色体末端的串联重复序列组成，可保护染色体 DNA 免受降解。端粒缩短是自然衰老的一部分；然而，生活应激、吸烟、药物使用、BMI 和精神障碍可能会破坏细胞衰老并影响端粒长度（TL）。在这种情况下，已有研究评估了饮酒对 TL 的影响；然而，结果不一致，这可能反映了不同的饮酒截止值和分类。
目的
为了阐明这一点，本研究探讨了 TL 与酒精使用障碍（AUD）、饮酒行为、终生压力和实际年龄的关系。
方法
使用定量 PCR 检测法从外周血 DNA 中定量测定端粒到白蛋白的比值（T/S 比值），该研究共纳入了来自国家酒精滥用和酒精中毒研究所（NIAAA）数据库的 260 名 AUD 患者和 449 名非依赖性健康对照者（HC）。
结果
与 HC 相比，AUD 患者的 TL 更短，年龄和 AUD 均为 TL 的独立预测因子，且 TL 与 AUD 之间存在显著的年龄交互作用。TL 还与 AUD 患者的冲动性有关。在 AUD 或 HC 中，我们均未观察到 TL 与酒精使用的慢性、摄入的酒精剂量或童年创伤暴露之间存在关联，尽管只有极少数 HC 报告了童年创伤史。
结论
我们的研究结果支持了之前关于慢性酒精暴露导致端粒缩短的发现，并表明 AUD 对 TL 的影响独立于年龄，且 TL 与 AUD 之间存在显著的年龄交互作用。这些发现与 AUD 患者的细胞加速衰老一致。
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