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4,8-dimethyl-non-7-en-4-ol | 97264-95-4

中文名称
——
中文别名
——
英文名称
4,8-dimethyl-non-7-en-4-ol
英文别名
4,8-Dimethyl-7-nonen-4-ol;4,8-dimethylnon-7-en-4-ol
4,8-dimethyl-non-7-en-4-ol化学式
CAS
97264-95-4
化学式
C11H22O
mdl
——
分子量
170.295
InChiKey
GLLYSEVWEKSIEI-UHFFFAOYSA-N
BEILSTEIN
——
EINECS
——
  • 物化性质
  • 计算性质
  • ADMET
  • 安全信息
  • SDS
  • 制备方法与用途
  • 上下游信息
  • 反应信息
  • 文献信息
  • 表征谱图
  • 同类化合物
  • 相关功能分类
  • 相关结构分类

计算性质

  • 辛醇/水分配系数(LogP):
    3.4
  • 重原子数:
    12
  • 可旋转键数:
    5
  • 环数:
    0.0
  • sp3杂化的碳原子比例:
    0.82
  • 拓扑面积:
    20.2
  • 氢给体数:
    1
  • 氢受体数:
    1

反应信息

点击查看最新优质反应信息

文献信息

  • Use of C.sub.8 -t-alkanols and C.sub.5 -C.sub.11 -omega-alken-1-ols in
    申请人:International Flavors & Fragrances Inc.
    公开号:US04764367A1
    公开(公告)日:1988-08-16
    Described are the uses of C.sub.8 -t-alkanols and C.sub.5 -C.sub.11 -omega-alken-1-ols taken alone or taken in combination as attractants house flies (Musca domestica L. (Diptera:Muscidae)). The C.sub.8 -t-alkanols and C.sub.5 -C.sub.11 -omega-alken-1-ols taken alone or in combination find utility primarily as bait enhancers for acute toxins and/or trapping devices.
    本文描述了C.sub.8 -t-烷醇和C.sub.5 -C.sub.11 -ω-烯烃-1-醇单独使用或组合使用作为诱蝇剂(家蝇(Musca domestica L.(双翅目:家蝇科))的吸引剂的用途。C.sub.8 -t-烷醇和C.sub.5 -C.sub.11 -ω-烯烃-1-醇单独使用或组合使用主要用作急性毒素的诱饵增强剂和/或捕蝇器。
  • DNA adducts and human atherosclerotic lesions
    作者:Blanka Binková、Přemysl Strejc、Otta Boubelík、Zdena Stávková、Irena Chvátalová、Radim J. Šrám
    DOI:10.1078/1438-4639-00072
    日期:——
    It has been hypothesized that mutational events may be involved in the atherogenetic process and that at least a portion of atherosclerotic plaques may be the results of monoclonal proliferation of a single mutated smooth muscle cell (SMC). Therefore, atherosclerosis may be similar to carcinogenesis and may have an environmental etiology. We have analyzed bulky-aromatic DNA adducts in human thoracic aortas from mate subjects, aged between 30-60 years, who died suddenly or accidentally, and who had been examined by autopsy within 24 h after death. We found significantly (P < 0.001) higher DNA adduct levels in the samples from subjects with frequent atherosclerotic changes in the whole body ("Cases", N = 76) compared with those having few atherosclerotic changes ("Controls", N = 57). We also observed a significantly elevated weight of heart and plasma levels of total and LDL cholesterol in "Cases" vs "Controls". Significant differences in DNA adduct levels between smokers and nonsmokers were observed in "Controls" only. Multivariate linear regression analyses with age-adjusted data confirmed a significant influence of LDL cholesterol (P < 0.001), vitamin A (P < 0.01), smoking behavior (P < 0.05; evaluated as plasma cotinine levels) and NAT2 genotypes (P < 0.05) on bulky-aromatic DNA adduct levels. The induction of DNA adducts suggests that alterations at the DNA level may contribute to the development of atherosclerosis. Furthermore, atherogenesis and carcinogenesis may share a similar etiology, i.e. genotoxic action of environmental chemicals.
  • Grignard; Escourrou, Comptes Rendus Hebdomadaires des Seances de l'Academie des Sciences, 1923, vol. 176, p. 1860
    作者:Grignard、Escourrou
    DOI:——
    日期:——
  • Escourrou, Bulletin de la Societe Chimique de France, 1926, vol. <4> 39, p. 1465
    作者:Escourrou
    DOI:——
    日期:——
  • Escourrou, Bulletin de la Societe Chimique de France, 1928, vol. <4>43, p. 1108
    作者:Escourrou
    DOI:——
    日期:——
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