Voluntary exercise and experimental mammary cancer.
Voluntary exercise and experimental mammary cancer.
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自愿锻炼和实验性乳腺癌。
DOI：
10.1007/978-1-4684-7953-9_5
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发表时间：
1992
影响因子：
--
通讯作者：
Zang,E
中科院分区：
文献类型：
--
作者：
Cohen,LA;Boylan,E;Epstein,M;Zang,E
流行病学和实验研究都表明，体育锻炼可以预防几种形式的癌症。对于实验性乳腺癌，运动已被证明可以促进或抑制肿瘤的发生，具体取决于所采用的活动类型。自愿运动，持续抑制，而强迫运动根据实验条件增强或抑制。本研究探讨了自发活动对两种不同化学诱导性乳腺肿瘤[亚硝基甲基脲(NMU)和7，12-二甲基苯并(A)蒽(DMBA)]、病毒诱导的小鼠乳腺肿瘤和可移植的转移性乳腺肿瘤(R-13672)的保护作用。其目的是确定能量消耗的保护作用是物种、品系、致癌物、饮食或阶段特有的现象，还是影响乳腺癌发生的所有方面的普遍现象。这些研究的结果表明，在高脂(HF)20-23%wt/wt的条件下，自愿运动既能抑制NMU和DMBA诱导的小鼠乳腺肿瘤的发展，也能抑制MMTV诱导的小鼠乳腺肿瘤的发展。R13762模型研究的结果不太清楚。在HF条件下，自愿运动对退休育种者的肺转移的促进作用在统计学上并不显著，但在中等脂肪(MF，11.5%wt/wt)条件下具有相反的效果。当只将最活跃的一半HF动物与久坐不动的对照组进行比较时，发现肺转移的统计学显著增强。这些研究表明，就初级预防而言，启动后阶段的自愿活动抑制了乳腺癌的发展，无论是化学诱导的还是病毒诱导的。关于二级预防，在HF条件下，活动可以增加肺转移的体积和数量，而在MF条件下可能发生相反的情况，表明饮食脂肪(能量摄入)和活动(能量消耗)之间的相互作用可能在确定体力活动对转移过程的影响方面发挥重要作用。有待阐明的是运动的程度和数量的影响，活动对致癌起始和进展阶段的影响，脂肪摄入、活动和乳腺癌发生之间相互作用的性质，以及最终导致体育运动保护作用的潜在细胞机制。
Both epidemiologic and experimental studies suggest that physical activity may protect against several forms of cancer. Regarding experimental mammary cancer, exercise has been shown to enhance or inhibit tumorigenesis depending on the type of activity employed. Voluntary exercise, consistently inhibited while forced exercise either enhanced or inhibited depending on experimental conditions. The present study explored the protective role of voluntary activity on two different kinds of chemically induced mammary tumors, [Nnitrosomethylurea(NMU) and 7,12-dimethylbenz(a)anthracene (DMBA)], a virally induced mouse mammary tumor (MMTV) and a transplantable metastasizing mammary tumor (R 13672). Its purpose was to determine whether the protective effect of energy expenditure was a species-, strain-, carcinogen-, diet-, or stage-specific phenomenon, or whether it was a general phenomenon affecting all aspects of mammary carcinogenesis. The results of these studies indicate that voluntary exercise inhibits the development of both the NMU- and DMBA-induced mammary tumors and the MMTV-induced mouse mammary tumor under high-fat (HF) 20–23% wt/wt) conditions. The results in the R13762 model study were less clear. Under HF conditions, voluntary exercise exerted a statistically insignificant enhancement of pulmonary metastases in retired breeders, but had the opposite effect in medium-fat (MF, 11.5% wt/wt) conditions. When only the most active half of the HF animals were compared to sedentary controls, a statistically significant enhancement of pulmonary metastases was found. These studies indicate that, with regard to primary prevention, voluntary activity during the post-initiation phase inhibits mammary tumor development whether chemically or virally induced. With regard to secondary prevention, under HF conditions, activity may enhance both the volume and number of lung metastasis, while the converse may occur under MF conditions, indicating that interactions between dietary fat (energy intake) and activity (energy expenditure) may play an important role in determining the effects of physical activity on the metastatic process. Remaining to be clarified are the effects of the degree and amount of exercise, the effects of activity on the initiation and progression phases of carcinogenesis, the nature of the interaction between fat intake, activity and mammary carcinogenesis, and, lastly, the underlying cellular mechanisms responsible for the protective effects of physical exercise.