Department of Basic Medical Sciences, Western University of Health Sciences, College of Osteopathic Medicine of the Pacific-Northwest, Lebanon, OR 97355, USA.
Department of Neurology, Psychiatry, and Radiation Medicine, Division of Neuroscience Oregon National Primate Research Center, Oregon Health & Science University, Beaverton, OR 97006, USA.
Mil Med. 2023 Nov 8;188(Suppl 6):575-583. doi: 10.1093/milmed/usad247.
Around 21.6-35% of military personnel are smokers, while 12.26% of them have been regularly exposed to second-hand smoke (SHS). Second-hand smoke is considered an important risk factor for neurological diseases because it can induce oxidative stress, DNA damage, and disrupt DNA repair pathways.
The brain of air (sham) or SHS exposed mice was cryoperserved, sectioned, and placed on a glass slide before immunoprobing them with antibodies to observe for oxidative DNA damage (8-oxoG), oxidative DNA repair (8-oxoguanine DNA glycosylase 1, Ogg1; apurinic/apyrimidinic endonuclease, Ape1), and inflammatory (glial fibrillary acidic protein) proteins.
Nissl staining of the prefrontal cortex (PFCTX) revealed the presence of dark, shrunken cells, hippocampal thinning, and the presence of activated astrocytes in SHS exposed mice. 8-oxoG staining was also more prominent in the PFCTX and hippocampus (HIPP) of SHS exposed mice. Ogg1 staining was reduced in the PFCTX and CA3 hippocampal neurons of SHS exposed mice, whereas it was more prominent in CA1 and CA4 hippocampal neurons. In contrast, Ape1 staining was more prominent in the PFCTX and the HIPP of SHS exposed mice.
These studies demonstrate that oxidative DNA damage (8-oxoG) was elevated and oxidative DNA repair (Ape1 and Ogg1) was altered in the brain of SHS exposed mice. In addition, activated astrocytes (i.e., glial fibrillary acidic protein) were also observed in the brain of SHS exposed mice. Therefore, SHS induces both oxidative DNA damage and repair as well as inflammation as possible underlying mechanism(s) of the cognitive decline and metabolic changes that were observed in chronically exposed mice. A better understanding of how chronic exposure to SHS induces cognitive dysfunction among military personnel could help improve the combat readiness of U.S. soldiers as well as reduce the financial burden on the DOD and veterans' families.
约 21.6-35%的军人是吸烟者，而其中 12.26%的人经常接触二手烟（SHS）。二手烟被认为是神经疾病的一个重要危险因素，因为它会引起氧化应激、DNA 损伤，并破坏 DNA 修复途径。
空气（假）或 SHS 暴露小鼠的大脑被冷冻保存，切片，然后放在载玻片上，用抗体免疫探测，观察氧化 DNA 损伤（8-oxoG）、氧化 DNA 修复（8-氧鸟嘌呤 DNA 糖基化酶 1，Ogg1；脱嘌呤/脱嘧啶内切酶，Ape1）和炎症（胶质纤维酸性蛋白）蛋白。
前额叶皮层（PFCTX）的尼氏染色显示，SHS 暴露小鼠的细胞出现深色、皱缩，海马变薄，星形胶质细胞激活。SHS 暴露小鼠的 PFCTX 和海马（HIPP）中 8-oxoG 染色也更为明显。Ogg1 染色在 SHS 暴露小鼠的 PFCTX 和 CA3 海马神经元中减少，而在 CA1 和 CA4 海马神经元中更为明显。相比之下，Ape1 染色在 SHS 暴露小鼠的 PFCTX 和 HIPP 中更为明显。
这些研究表明，氧化 DNA 损伤（8-oxoG）在 SHS 暴露小鼠的大脑中升高，氧化 DNA 修复（Ape1 和 Ogg1）发生改变。此外，在 SHS 暴露小鼠的大脑中还观察到激活的星形胶质细胞（即胶质纤维酸性蛋白）。因此，SHS 可能通过诱导氧化 DNA 损伤和修复以及炎症，作为慢性暴露小鼠认知能力下降和代谢变化的潜在机制。更好地了解慢性接触 SHS 如何导致军人认知功能障碍，有助于提高美国士兵的战备能力，并减轻国防部和退伍军人家庭的经济负担。
