Carrots may have a profound and substantial effect in reducing the risk, progression, and treatment of skin cancer, some scientists suggested.
Skin cancer is a condition characterized by cell growth disorderly and uncontrollably in skin tissue. At the later stage, the cancerous cells may infect other healthy tissue and organ a distance away from the original site.
Carrot, a root vegetable with orange color is a subspecies of Daucus carota, belongings to the family Apiaceae, native to Asia and Europe.
In the investigation of essential oil isolated from wild carrot umbels effect in mice induced skin cancer through injection of 7,12-dimethyl benz(a)anthracene (DMBA), after 20 weeks of administered to animals via gavage (0.02 mL of 100% oil), intraperitoneal (0.3 mL of 2% oil), and topical (0.2 mL of 5, 50, and 100% oil) with half-maximal inhibitory concentration IC50, researchers showed that topical administration of 100% mice group exerted in delay skin cancer appearance and inhibited tumor incidence of 89%.
With the concentration of IC40, topical 50% and 5% treatment inhibited tumor incidence by 83% and 36%, respectively.
Topical ingestion of 100, 50, and 5% oil, also revealed a significant decrease of tumor volume by 99, 91, and 70%, respectively.
Intraperitoneally, treatment mice displayed an inhibited tumor by 43% and decreased tumor volume by 85%, whereas gavage treatment showed minimal effects on both.
These results suggested that intraperitoneal and topical treatment of wild carrot essential oil decreased infiltration and proliferation with an increase in abnormal thickening of the outer layer of the skin.
Further analysis of the wild carrot essential oil anti-cancer effect on human epidermal keratinocytes and the chemopreventive activity of the pentane diethyl ether fraction on DMBA/TPA-induced skin carcinogenesis in mice, scientists in the joint study lead by the Lebanese American University suggested that application of all fractions isolated from the essential oil exhibited significant cytotoxicity, with HaCaT cells being 2.4-3 times less sensitive than HaCaT-ras A5 (benign tumorigenic), and HaCaT-ras II4 (malignant) cells observed by western blot.
In Gas chromatography-mass spectrometry, 2-himacharlen-6-ol. a derivative isolated from pentane/diethyl ether fraction (F2), demonstrated strong inhibition of HaCaT-ras A5 and HaCaT-ras II4 cells through cell cycle arrest in the accumulation of cells of the sub-G1 apoptotic phase and apoptosis in decreased the population of cells in the S and G2/M phases.
These results were attributed to the F2 fraction in enhanced expression of pro-apoptotic (Bax) in induction cellular apoptosis and attenuated expression of anti-apoptotic (Bcl2) proteins in promoted cancer proliferation.
Interestingly, all fractions also decreased the phosphorylation of AKT, (AKT is an essential component of the PI3K (phosphatidylinositol 3-kinase pathway) in monitoring skin cancer cell growth and resistance to apoptosis and ERK(components of mitogen-Activated Protein Kinase (MAPK) signaling pathways) in mediated different anti-proliferative events, such as apoptosis, autophagy, and senescence.
Based on the information fonding, Dr. Shebaby WN, the lead author said, " F2 fraction has remarkable antitumor activity against DMBA/TPA-induced skin carcinogenesis, an effect that may be mediated through inhibition of the MAPK/ERK and PI3K/AKT pathways".
The above differentiation was supported by the joint study led by the University of Surrey in the evaluation of Daucus carota oil extract (DCOE) activity in the inhibition of HaCaT-ras II-4 epidermal squamous cells.
According to the experiment, β-2-himachalen-6-ol isolated from the wild carrot essential oil at dose-dependent decreased in skin cell survival with an IC50 and IC90 of 8 and 30 μg/ml, respectively.
Observation of Flow cytometry analysis also revealed that treatment of β-2-himachalen-6-ol is linearly associated with volume injection, as the dose of 10 μg/ml HC significantly increased the number of cells undergoing late apoptosis (28%), while 25 μg/ml caused a larger cell shift towards late apoptosis (46.6%) and necrosis (39%).
Besides decreasing the phosphorylation of AKT, and ERK as shown in the mentioned above, β-2-himachalen-6-ol also inhibited the significant decrease in protein levels of p53 and Bcl-2 in acting as tumors suppressor, caused by 7,12-Dimethylbenz[a]anthracene (DMBA)/ 12-O-tetradecanoylphorbol-13-acetate (TPA) and increased p21 and Bax function in cell cycle arrest and activation of apoptosis.
Astonishingly, the application of essential oil extract from wild carrot inhibited skin cancer proliferation and induced apoptosis withing harming the nearby healthy cells in tested mice.
Taken together, the essential oil of carrot and its bioactive derivative may be considered as an adjunct therapy in reduced risk, and progression and used a combination with standard medicine for the treatment of skin cancer.
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Author Biography
Kyle J. Norton (Scholar, Master of Nutrients, All right reserved)
Health article writer and researcher; Over 10.000 articles and research papers have been written and published online, including world wide health, ezine articles, article base, health blogs, self-growth, best before it's news, the karate GB daily, etc.,.
Named TOP 50 MEDICAL ESSAYS FOR ARTISTS & AUTHORS TO READ by Disilgold.com Named 50 of the best health Tweeters Canada - Huffington Post
Nominated for shorty award over last 4 years
Some articles have been referenced in medical research, such as the international journal Pharma and Bio Science, ISSN 0975-6299.
Sources
(1) Chemopreventive effects of wild carrot oil against 7,12-dimethyl benz(a)anthracene-induced squamous cell carcinoma in mice by Zeinab RA1, Mroueh M, Diab-Assaf M, Jurjus A, Wex B, Sakr A, Daher CF(PubMed)
(2) Wild carrot pentane-based fractions suppress proliferation of human HaCaT keratinocytes and protect against chemically-induced skin cancer by Shebaby WN1, Mroueh MA2, Boukamp P3,4, Taleb RI1, Bodman-Smith K5, El-Sibai M1, Daher CF(PubMed)
(3) β-2-himachalen-6-ol protects against skin cancer development in vitro and in vivo by Daaboul HE1, Daher CF2, Taleb RI2, Boulos J2, Bodman-Smith K1, Boukamp P3,4, Shebaby WN2, Dagher C5, El-Sibai M2, Mroueh MA(PubMed)
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