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首页> 外文期刊>Pharmacology and Toxicology: An International Journal >In vitro cytotoxicity of protocatechuic acid to cultured human cells from oral tissue: involvement in oxidative stress.
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In vitro cytotoxicity of protocatechuic acid to cultured human cells from oral tissue: involvement in oxidative stress.

机译：原儿茶酸对口腔组织中培养的人细胞的体外细胞毒性：参与氧化应激。

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Data on the biologic activity of protocatechuic acid are contradictory; some studies have shown that it acts as an antioxidant and suppresses chemical-induced carcinogenesis and others that it induces oxidative stress and promotes tumour formation. The anticarcinogenicity of protocatechuic acid was postulated to be related, in part, to its specific suppression of neoplastic hyperproliferation. To determine whether protocatechuic acid was preferentially antiproliferative to malignant cells, non-malignant and carcinoma cells were exposed for 24 hr to protocatechuic acid (2.5 to 25 mM) and viability was assessed with the neutral red assay. The cell lines were derived from tissues of the human oral cavity, the initial site of exposure upon ingestion of dietary protocatechuic acid, and included normal GN61 gingival fibroblasts, immortalized, non-tumorigenic S-G gingival epithelial cells, and malignant HSG1 cells derived from the salivary gland, HSC-2 cells from the floor of the oral cavity, and CAL27 cells from the tongue. Selective toxicity of protocatechuic acid to malignant cells was not observed. Furthermore, using a total cellular protein determination to quantitate cell growth, no differences in comparative sensitivities of S-G epithelial cells and HSG1 carcinoma cells were noted in a 3 day continuous exposure to 2.5 to 12.5 mM protocatechuic acid and in recovery from a 24 hr exposure to 3 to 15 mM protocatechuic acid. The S-G and HSG1 cells were then used to study the effects of elevated concentrations of protocatechuic acid on oxidative stress. For both cell types, protocatechuic acid induced oxidative stress, presumably through its bioactivation by a tyrosinase pathway. A brief exposure to 25 mM protocatechuic acid lowered the levels of intracellular glutathione and potentiated Fe2+-induced lipid peroxidation of the cells. As determined with the neutral red assay, S-G and HSG1 cells exposed briefly to a non-toxic level (0.5 mM) of the glutathione depleter, 1,3-bis(2-chloroethyl)-N-nitrosourea, were hypersensitive to a subsequent challenge with 10 mM protocatechuic acid and preexposure of the S-G and HSG1 cells to a nontoxic level of protocatechuic acid (2.5 mM) enhanced their sensitivity to a subsequent exposure to tert-butyl hydroperoxide. These findings were consistent with protocatechuic acid, at high levels (> or = 10 mM), acting as an inducer of oxidative stress.
机译：原儿茶酸的生物活性数据相互矛盾。一些研究表明，它可作为抗氧化剂并抑制化学诱导的致癌作用，而另一些研究则可诱导氧化应激并促进肿瘤形成。据推测，原儿茶酸的抗癌性部分与其特异性抑制肿瘤过度增殖有关。为了确定原儿茶酸是否优先对恶性细胞抗增殖，将非恶性和癌细胞暴露于原儿茶酸（2.5至25 mM）24小时，并通过中性红分析评估其生存力。该细胞系来源于人口腔组织，摄入饮食性原儿茶酸的初始暴露部位，包括正常的GN61牙龈成纤维细胞，永生的，非致瘤性SG牙龈上皮细胞和唾液来源的恶性HSG1细胞。腺体，来自口腔底部的HSC-2细胞和来自舌头的CAL27细胞。没有观察到原儿茶酸对恶性细胞的选择性毒性。此外，使用总细胞蛋白测定来定量细胞生长，在连续暴露于2.5至12.5 mM的原儿茶酸中3天以及从暴露于24小时的SG中，SG上皮细胞和HSG1癌细胞的比较敏感性没有差异。 3至15 mM的原儿茶酸。然后将S-G和HSG1细胞用于研究原儿茶酸浓度升高对氧化应激的影响。对于这两种细胞类型，原儿茶酸都可能通过酪氨酸酶途径进行生物激活，从而诱导氧化应激。短暂暴露于25 mM的原儿茶酸可降低细胞内谷胱甘肽的水平，并增强Fe2 +诱导的细胞脂质过氧化作用。根据中性红分析测定，SG和HSG1细胞短暂暴露于无毒水平（0.5 mM）的谷胱甘肽耗竭剂1,3-双（2-氯乙基）-N-亚硝基脲，对随后的挑战过敏用10 mM的原儿茶酸和SG和HSG1细胞预先暴露于无毒水平的原儿茶酸（2.5 mM）可以增强其对随后暴露于叔丁基过氧化氢的敏感性。这些发现与高水平（>或= 10 mM）的原儿茶酸一致，可作为氧化应激的诱导剂。

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