Ácido ascórbico na prevenção e no tratamento do câncer

Mata, Ana Maria Oliveira Ferreira da; Carvalho, Ricardo Melo de; Alencar, Marcus Vinícius Oliveira Barros de; Cavalcante, Ana Amélia de Carvalho Melo; Silva, Benedito Borges da

doi:10.1590/1806-9282.62.07.680

Brazil

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REVIEW ARTICLES • Rev. Assoc. Med. Bras. 62 (7) • Out 2016 • https://doi.org/10.1590/1806-9282.62.07.680 linkcopiar

Ácido ascórbico na prevenção e no tratamento do câncer

Autoria SCIMAGO INSTITUTIONS RANKINGS

Resumo

Este estudo de revisão teve como objetivo fazer o mapeamento sistemático do ácido ascórbico na prevenção e/ou no tratamento do câncer como antioxidante e/ou pró-oxidante em estudos clínicos e não clínicos, entre 2011 e 2015, para o entendimento das variações de dose-resposta, bem como dos seus mecanismos de ação como agente antioxidante e antitumoral. Nas bases de dados Pubmed e Bireme, foram identificados 78 artigos, dos quais apenas 30 apontavam o ácido ascórbico na prevenção e/ou no tratamento do câncer. Contudo, há controvérsias sobre as doses utilizadas e faltam estudos clínicos que caracterizem melhor o seu mecanismo de ação. Outros estudos devem ser realizados para o entendimento das variações de dose-resposta, bem como de seus mecanismos de ação, como agente antioxidante ou antitumoral, para auxiliar o tratamento e a prevenção do câncer, visando à melhor qualidade de vida dos pacientes e da população em geral.

Palavras-chave:
neoplasias; câncer; prevenção; ácido ascórbico; antioxidantes

Study type	Type of cancer/cell	Mechanism of action	Dose/concentration	References
Clinical	Pancreas, breast, kidney, lung, liver, bladder, lymphoma, prostate, colon, and stomach	Decrease in levels of C-reactive protein and proinflammatory cytokines	0.04-0.28 mM	⁽ ²⁵ ⁾
Non-clinical	Breast cancer in mice	Hinders metastases, tumor growth and secretion of inflammatory cytokines, and enhances tumoral encapsulation	0.85 mM	⁽ ²⁶ ⁾
Non-clinical	MCF-7 cells in breast cancer	Attenuation of cytotoxicity, decrease in apoptosis, protection of neoplastic cells against lipid peroxidation	0.05 and 0.5 mM	⁽ ²⁷ ⁾
Non-clinical	MCF-7 cells in breast cancer	Decrease in cytotoxicity	0.1 mM	⁽ ²⁸ ⁾
Clinical	Pancreas, breast, kidney, lung, liver, bladder, lymphoma, prostate, colon, brain, leukemia, stomach, ovary, skin, and uterus	Decreased inflammation	1-10 mM	⁽ ²⁹ ⁾
Non-clinical	Cells from renal carcinoma	Anti-apoptotic activity by recruiting Bcl-2	0.11 and 2.28 mM	⁽ ³⁰ ⁾
Non-clinical	Cells from melanoma (B16FO)	Hinders metastases and tumor growth	4 mM	⁽ ³¹ ⁾
Non-clinical	Cells from cervical cancer (HeLa)	Modulation of markers for cancer proliferation (Ki67), invasion and metastasis (MMP-2 and -9), angiogenesis (VEGF), apoptosis (TUNEL and Bcl-2), and inflammation (COX-2, iNOS and GSTπ)	4 mM	⁽ ³² ⁾
Non-clinical	Lung cancer in ferrets	Protection against lung injury induced by exposure to cigarette smoke, by inhibiting the expression of cyclin D1	1.2 mM	⁽ ³³ ⁾
Non-clinical	Cells from neuroblastoma	Anti-apoptotic activity	0.1-0.4 mM	⁽ ³⁴ ⁾
Non-clinical	Cells from acute lymphoblastic leukemia	Decreased production of reactive oxygen species caused by 4-(hydroxyphenyl) retinamide (4-HPR)	100 µM	⁽ ³⁵ ⁾
Non-clinical	Cells from osteosarcoma (143-B)	Limitation of the invasive potential	0.28 mM	⁽ ³⁶ ⁾

Study type	Type of cancer/cell	Mechanism of action	Dose/concentration	References
Non-clinical	Cells from ovarian cancer (IOSE-385, OVCAR-3, SKOV-3 and OVCA-432)	Inhibition of cell progression by increasing the levels of H₂O₂	0.25 mM	⁽ ³⁷ ⁾
Non-clinical	Different cell lines	Antiproliferative effect on tumor cells, through interference with cell cycle (G₀/G₁) and production of H₂O₂	0.1-2 mM	⁽ ³⁸ ⁾
Non-clinical	AGS cells	Inhibition of cell progression, cytotoxicity, modification of proteins related to apoptosis	0.3 mM	⁽ ³⁹ ⁾
Non-clinical	Esophageal squamous cells and Barrett’s esophagus cells (CP-A, CP-B, CP-C and CP-D)	Decreased cell growth	0.5 mM	⁽ ⁴⁰ ⁾
Non-clinical	Cells from gastric (23132/87), colon (HT-29), ovary (SKOV-3), pancreas (BXPC-3) and breast (BT-20, MDA-MB-468, MDA-MB-231 and MCF-7) carcinoma, glioblastoma (U-13898, U-87 and U-251), endothelial cells (HUVEC) and fibroblasts (NHDF)	Production of H₂O₂	0.005-0.1 mM	⁽ ⁴¹ ⁾
Non-clinical	Cells from cervical cancer (HeLa)	Decreased cell growth	4 mM	⁽ ³² ⁾
Non-clinical	Colon carcinoma in mice	Decreased levels of serotonin, increased level of hemorrhagic necrosis and permeability of the endothelium	28.39 mM	⁽ ⁴² ⁾
Non-clinical	Laryngeal carcinoma (HEp-2)	Production of reactive oxygen species through the release of Ca₂⁺	3-10 mM	⁽ ⁴³ ⁾
Non-clinical	Cells from neuroblastoma	Induction of apoptosis	1-6 mM	⁽ ³⁴ ⁾
Non-clinical	Cells from pancreatic cancer (PANC-1, AsPC-1, BxPC-3 and MIA PaCa-2)	Aponecrosis induced in cells resistant to apoptosis	4.26 mM	⁽ ⁴⁴ ⁾
Non-clinical	Cells from Epstein-Barr virus-positive Burkitt’s lymphoma and lymphoblastoid cells	Production of reactive oxygen species and induction of cell death	22.71 mM	⁽ ⁴⁵ ⁾
Non-clinical	Cells from neuroblastoma (SK-N-MC) in vitro and in vivo	in vitro – induction of apoptosis, inhibition of cell proliferation, secretion of MMP-2 and -9, and increased secretion of TIMP-2in vivo – inhibition of tumor growth	Not reported	⁽ ⁴⁶ ⁾
Clinical	Metastatic pancreatic cancer	Decreased tumor size	0.28; 0.43 and 0.5 mM	⁽ ⁴⁷ ⁾
Non-clinical	Cells from prostate cancer (PC3) in mice	Production of reactive oxygen species, induced autophagy, tumor suppression	0.4 mM	⁽ ⁴⁸ ⁾
Non-clinical	Cells from malignant pleural mesothelioma in rats	in vitro – synergism in the mechanism of cytotoxicityin vivo – blocking of tumor progression and metastasis, reduction in tumor size	11.36 mM	⁽ ⁴⁹ ⁾
Non-clinical	Epithelial cells from lung cancer (NSCLC)	Induction of cell death by activation of apoptosis and via mechanism of production of reactive oxygen species, loss of cell viability	0.5-5 mM	⁽ ⁵⁰ ⁾
Non-clinical	Solid Ehrlich carcinoma in mice	Inhibition of tumor growth and increased expression of p53	0.68 mM	⁽ ⁵¹ ⁾
Non-clinical	Cells from colon cancer (RKO and SW480)	Decreased cell proliferation, induced apoptosis and necrosis, down-regulation of proteins (Sp1, Sp3 e Sp4) and decreased expression of genes that involve cell proliferation and angiogenesis	1-3 mM	⁽ ⁵² ⁾

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