乙酸视黄酯（10 μM）抑制细胞生长（如黑色素瘤细胞系 B 16 和 S91，抑制率分别为 48% 和 79%）[2]。

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本研究评估了retinyl acetate（浓度为10⁻⁵ M）在体外对31种未转化、转化和肿瘤细胞系的生长抑制作用。根据敏感性对细胞进行分类：(a) 不受retinyl acetate影响（抑制率<10%）或仅轻微抑制（抑制率<25%）的细胞，包括未转化的BHK和CHO-K1-pro细胞、病毒转化的PyBHK、人纤维肉瘤HT1080，以及其他如未转化的Balb/3T3、SV3T3、MSV3T3和化学转化的BP3T3。(b) 生长受到抑制（25-50%）的细胞，例如神经母细胞瘤C1300（抑制率40%）、小鼠乳腺腺癌M12和DD3、人乳腺癌肉瘤H,0578以及小鼠淋巴瘤S49和EL4。(c) 受到中度生长抑制（50-75%）的细胞，包括小鼠肉瘤S180、肥大细胞瘤P815（抑制率21%）、大鼠乳腺腺癌R3230AC等。(d) 对retinyl acetate极度敏感（生长抑制>75%）的细胞，例如小鼠黑色素瘤S91（抑制率79%）、大鼠乳腺腺癌13762NF、小鼠淋巴肉瘤RAW117等。在大多数情况下，维甲酸比retinyl acetate效力更强，但对于某些细胞系（例如C1300神经母细胞瘤、S91黑色素瘤、Mm5mT和13762NF乳腺腺癌），retinyl acetate的活性几乎相当。[2]

DMBA 产生的 Sprague-Dawley 肿瘤的进展受到乙酸视黄酯（饮食中 250 mg/kg）的抑制 [1]。

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在饮食中添加retinyl acetate（250 毫克/公斤饲料）能显著抑制N-甲基-N-亚硝基脲（NMU）诱导的雌性Sprague-Dawley大鼠乳腺致癌作用。在不同NMU剂量组中，它均降低了乳腺癌症（包括良性肿瘤）的发生率和总数量。此外，retinyl acetate显著延长了可触及乳腺肿瘤出现的潜伏期。例如，在接受高剂量NMU处理的大鼠中，与安慰剂对照组相比，首次出现可触及癌症的时间大约延长了一倍。在实验结束时（175天），接受低剂量NMU并喂食retinyl acetate的大鼠未发生乳腺癌症。[1]

采用标准化实验评估细胞生长抑制。简要流程：将细胞（0.5-1.0 x 10⁵个）接种于培养皿中的生长培养基内。实验组接受含有终浓度为10⁻⁵ M的retinyl acetate（溶解于0.1%乙醇中）的新鲜生长培养基。对照组仅接受含有0.1%乙醇的培养基。所有涉及类视黄醇的操作均在弱光下进行，培养皿用铝箔包裹。细胞在37°C、13% CO₂的湿润环境中培养。单层或多层培养物每三天更换一次新鲜培养基。悬浮培养通过向现有培养物中添加新鲜培养基进行补液。培养至对照组细胞接近汇合（通常5-6天），或对于悬浮细胞，直至对照组细胞经历五到六个复制周期。在终点时，使用不含钙和镁的PBS中的EDTA解离贴壁细胞，并使用电子粒子计数器或血球计数板进行计数。通过台盼蓝排除法评估细胞活力。增殖抑制百分比相对于对照组计算。实验至少重复两次，每次设双复孔。[2]

Female Sprague-Dawley rats, 42 days old, were used. At 50 days of age (average weight 150g), rats received an intravenous injection of NMU dissolved in physiological saline (adjusted to pH 5.0) at doses of 5.0, 2.5, or 1.25 mg per 100g body weight. A second injection of NMU or saline (for controls) was administered 7 days later. Three days after the second injection, all rats were placed on experimental diets for the remainder of the study. Retinyl acetate was blended into the standard stock diet in the form of stable gelatinized beadlets at a concentration of 250 mg per kg diet. Control groups received placebo beadlets without the retinoid. Rats were palpated twice weekly for mammary tumor detection, weighed twice weekly, and observed daily for signs of toxicity. All animals were sacrificed 175 days after the initial NMU injection, and mammary tumors were excised for histological examination. [1]

The article mentions that the carcinogen NMU has a half-life of only a few hours at human pH. However, the article does not describe the ADME or pharmacokinetic parameters of retinoic acid itself (e.g., absorption, distribution, metabolism, excretion, half-life, oral bioavailability). [1]

In this study, no signs of vitamin A overdose (retinoid toxicity) were observed in rats fed retinyl acetate. The body weight and liver histology of rats treated with retinyl acetate were essentially the same as those of rats in the placebo control group. Vaginal smears of rats fed retinyl acetate showed normal estrous cycles, indicating that there were no significant changes in ovarian steroid metabolism. The inhibitory effect on carcinogenicity was not due to the general toxicity of the compound. [1] In cell culture experiments, the growth inhibition induced by retinyl acetate was not due to direct cytotoxicity. Daily observation of cultures exposed to 10⁻⁵ M retinyl acetate showed no increase in cell debris or detached cells. During the experimental period (5–8 days), the survival rate of cells treated with retinoic acid was consistently above 90%, similar to the survival rate of untreated control cells. [2]

[1]. Retinyl acetate inhibits mammary carcinogenesis induced by N-methyl-N-nitrosourea. Nature. 1977 Jun 16;267(5612):620-1.

[2]. Lotan R, Nicolson GL. Inhibitory effects of retinoic acid or retinyl acetate on the growth of untransformed, transformed, and tumor cells in vitro. J Natl Cancer Inst. 1977 Dec;59(6):1717-22.

Retinyl acetate is an acetate ester. It is functionally related to all-trans retinol. Retinyl acetate is a natural fatty acid ester form of retinol (vitamin A) with potential antitumor and chemopreventive activities. Retinyl acetate can bind to and activate retinoid receptors, thereby inducing cell differentiation and inhibiting cell proliferation. This substance can also inhibit carcinogen-induced tumor transformation in certain cancer cell types and has immunomodulatory properties. (NCI04)

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Retinyl acetate is a retinoid (vitamin A analog). This study shows that retinyl acetate effectively prevents experimental breast cancer in an NMU-induced rat breast cancer model. Compared with other models (such as DMBA-induced cancer models), the NMU-induced breast cancer model is closer to human breast cancer in terms of invasiveness, hormone dependence, and metastasis. The mechanism by which vitamin A-like substances inhibit breast cancer development is not fully elucidated, but some studies suggest it may be related to maintaining normal epithelial cell differentiation. The authors noted that although no toxicity was observed in this study, the potential toxicity of retinyl acetate makes the development of novel synthetic vitamin A derivatives with higher activity and lower toxicity particularly important. [1] Retinyl acetate is a vitamin A derivative (vitamin A derivative). This study showed that it can directly inhibit the in vitro proliferation of a variety of transformed cell lines and tumor cell lines, suggesting that the antitumor activity of vitamin A derivatives observed in vivo may at least partly stem from its direct effect on tumor cell growth, rather than just indirect mechanisms such as immune regulation. Its mechanism of action is not fully elucidated, but may involve interaction with specific intracellular binding proteins, thereby affecting DNA synthesis. Different cell lines have different sensitivities to vitamin A derivatives, suggesting that screening tumor cells for vitamin A derivatives in vitro may help predict their potential response to vitamin A derivative therapy. [2]

C22H32O2

328.4883

328.24

127-47-9

Retinyl acetate-d4;118139-40-5

638034

Light yellow to yellow solid powder

1.0±0.1 g/cm3

440.5±14.0 °C at 760 mmHg

57-58 °C

124.8±18.5 °C

0.0±1.1 mmHg at 25°C

1.532

7.39

26.3

0

2

7

24

596

0

CC1=C(C(CCC1)(C)C)/C=C/C(=C/C=C/C(=C/COC(=O)C)/C)/C

QGNJRVVDBSJHIZ-QHLGVNSISA-N

InChI=1S/C22H32O2/c1-17(9-7-10-18(2)14-16-24-20(4)23)12-13-21-19(3)11-8-15-22(21,5)6/h7,9-10,12-14H,8,11,15-16H2,1-6H3/b10-7+,13-12+,17-9+,18-14+

[(2E,4E,6E,8E)-3,7-dimethyl-9-(2,6,6-trimethylcyclohexen-1-yl)nona-2,4,6,8-tetraenyl] acetate

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

DMSO : ~50 mg/mL (~152.21 mM)
H2O : ~0.67 mg/mL (~2.04 mM)

配方 1 中的溶解度: ≥ 2.5 mg/mL (7.61 mM) (饱和度未知) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (这些助溶剂从左到右依次添加，逐一添加), 澄清溶液。
例如，若需制备1 mL的工作液，可将100 μL 25.0 mg/mL澄清DMSO储备液加入到400 μL PEG300中，混匀；然后向上述溶液中加入50 μL Tween-80，混匀；加入450 μL生理盐水定容至1 mL。
*生理盐水的制备：将 0.9 g 氯化钠溶解在 100 mL ddH₂O中，得到澄清溶液。

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配方 2 中的溶解度: ≥ 2.08 mg/mL (6.33 mM) (饱和度未知) in 10% DMSO + 90% Corn Oil (这些助溶剂从左到右依次添加，逐一添加), 澄清溶液。
例如，若需制备1 mL的工作液，可将 100 μL 20.8 mg/mL 澄清 DMSO 储备液加入到 900 μL 玉米油中并混合均匀。

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配方 3 中的溶解度: 2 mg/mL (6.09 mM) in PBS (这些助溶剂从左到右依次添加，逐一添加), 澄清溶液; 超声助溶 (<60°C).

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请根据您的实验动物和给药方式选择适当的溶解配方/方案：
1、请先配制澄清的储备液(如：用DMSO配置50 或 100 mg/mL母液(储备液));
2、取适量母液，按从左到右的顺序依次添加助溶剂，澄清后再加入下一助溶剂。以 下列配方为例说明 (注意此配方只用于说明，并不一定代表此产品 的实际溶解配方):
10% DMSO → 40% PEG300 → 5% Tween-80 → 45% ddH2O (或 saline);
假设最终工作液的体积为 1 mL, 浓度为5 mg/mL: 取 100 μL 50 mg/mL 的澄清 DMSO 储备液加到 400 μL PEG300 中，混合均匀/澄清；向上述体系中加入50 μL Tween-80，混合均匀/澄清；然后继续加入450 μL ddH2O (或 saline)定容至 1 mL；
3、溶剂前显示的百分比是指该溶剂在最终溶液/工作液中的体积所占比例;
4、 如产品在配制过程中出现沉淀/析出，可通过加热(≤50℃)或超声的方式助溶;
5、为保证最佳实验结果，工作液请现配现用！
6、如不确定怎么将母液配置成体内动物实验的工作液，请查看说明书或联系我们;
7、 以上所有助溶剂都可在 Invivochem.cn网站购买。