Protective effects of purple carrot extract (Daucus carota) against rat tongue carcinogenesis induced by 4-nitroquinoline 1-oxide

Soares, Gláucia Resende; Moura, Carolina Foot Gomes de; Silva, Marcelo José Dias; Vilegas, Wagner; Santamarina, Aline Boveto; Pisani, Luciana Pellegrini; Estadella, Débora; Ribeiro, Daniel Araki

doi:10.1007/s12032-018-1114-7

Cited by 20 publications

(9 citation statements)

References 57 publications

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“…Upon euthanization; tongues had normal histological features with no inflammatory, or atypical changes. These results were in agreement with other studies that reported the same findings on control group when the same model was used (4,19) .…”

Section: Discussionsupporting

confidence: 93%

Synergistic Therapeutic Effect of Honokiol and 5-Fluorouracil on the Induced-Tongue Cancer in Rats.

Swidan

Hassan

mansy

2021

Dental Science Updates

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Introduction: 5-Fluorouracil (5-FU) is a common chemotherapeutic drug for treatment of oral squamous cell carcinoma. However, its toxicity to normal tissues has limited its role as an effective cancer therapy. Aim: This research aimed to investigate the effect of combining 5-FU with honokiol (HNK) on enhancing the anticancer activity of 5-FU without increasing its toxicity. Material and methods: HNK was used in combination with 5-FU for treatment of tongue carcinoma induced chemically by 4-nitroquinoline 1 oxide (4-NQO) in albino rats. Rats were divided into five groups (10 animals each) including control, 4-NQO, 5-FU, HNK, and combined 5-FU with HNK. Serial sections of the tongues from all animals were examined microscopically and real-time PCR quantification of P53 gene expression was also assessed. Results: The results showed that treatment with both 5-FU + HNK had significantly regressed the number and size of malignant lesions seen in the carcinogen-only group. Data analysis revealed a statistically significant decrease in the expression levels of mutant P53 in the combined treatment group compared to control groups. Conclusion: This study reported that HNK and 5-FU had a synergistic cytotoxic effect on this model, without notable intensification of the side effects associated with 5-FU treatment.

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Section: Discussionsupporting

confidence: 93%

Synergistic Therapeutic Effect of Honokiol and 5-Fluorouracil on the Induced-Tongue Cancer in Rats.

Swidan

Hassan

mansy

2021

Dental Science Updates

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“…In oral cancer patients, elevated salivary 8OHdG levels have already been related to tumor progression and also seem to be involved in the pathogenesis of the disease 30 , 31 . The increased 8OHdG immunoexpression in non-tumor tissues contribute to the chemical oral carcinogenesis in preclinical models 32 , 33 .…”

Section: Discussionmentioning

confidence: 99%

Stress hormones promote DNA damage in human oral keratinocytes

Valente

Cardoso

Kayahara

et al. 2021

Sci Rep

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Chronic stress increases the systemic levels of stress hormones norepinephrine and cortisol. As well as tobacco-specific carcinogen NNK (4-(methylnitrosamine)-1-(3-pyridyl)-1-butanone), they can induce expressive DNA damage contributing to the cancer development. However, it is unknown whether stress hormones have genotoxic effects in oral keratinocytes. This study investigated the effects of stress hormones on DNA damage in a human oral keratinocyte cell line (NOK-SI). NOK-SI cells stimulated with norepinephrine or cortisol showed higher DNA damage compared to untreated cells. Norepinephrine-induced DNA damage was reversed by pre-treatment with beta-adrenergic blocker propranolol. Cells treated with NNK combined to norepinephrine displayed reduced levels of caspases 3 and 7. Cortisol also reduced the activity of pro-apoptotic enzymes. NNK or norepinephrine promoted single-strand breaks and alkali-label side breaks in the DNA of NOK-SI cells. Pre-treatment of cells with propranolol abolished these effects. Carcinogen NNK in the presence or absence of cortisol also induced DNA damage of these cells. The genotoxic effects of cortisol alone and hormone combined with NNK were blocked partially and totally, respectively, by the glucocorticoid receptor antagonist RU486. DNA damage promoted by NNK or cortisol and carcinogen combined to the hormone led to intracellular γH2AX accumulation. The effects caused by NNK and cortisol were reversed by propranolol and glucocorticoid receptor antagonist RU486, respectively. Propranolol inhibited the oxidation of basis induced by NNK in the presence of DNA-formamidopyrimidine glycosylase. DNA breaks induced by norepinephrine in the presence or absence of NNK resulted in higher 8OHdG cellular levels. This effect was also induced through beta-adrenergic receptors. Together, these findings indicate that stress hormones induce DNA damage of oral keratinocytes and could contribute to oral carcinogenesis.

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“…Immunohistochemistry was made according to Soares et al 26 For this, serial sections of 4 μm were deparaffinized in xylene, rehydrated in ethanol, and incubated in a microwave with 10 mM citric acid buffer (pH = 6) for three cycles of 5 minutes each for antigen retrieval. The following primary antibodies were used: matrix metalloproteinases-2 (MMP-2) mouse monoclonal anti-rat antibody (1:50) (8B4), MMP-9 mouse monoclonal anti-rat antibody (1:100) (2C3) and 8-hydroxydeoxyguanosine (8OHdG) mouse monoclonal anti-rabbit antibody (1:100) (B1712) Santa Cruz Biotechnology, CA.…”

Section: Immunohistochemistrymentioning

confidence: 99%

Therapeutical effects of vaccine from Trypanosoma cruzi amastigote surface protein 2 by simultaneous inoculation with live parasites

Ribeiro

Ferreira

Machado

et al. 2018

J of Cellular Biochemistry

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The aim of this study was to evaluate the efficacy of vaccine using replicationdeficient human recombinant Type 5 replication-defective adenoviruses (AdHu5) carrying sequences of the amastigote surface protein 2 (ASP2) (AdASP2) in mice infected with the Trypanosoma cruzi (T cruzi) Y strain. A total of 16 A/Sn mice female were distributed into four groups, as follows (n = 4 per group): Group 1 -Control Group (CTRL); Group 2 -Infected Group (TC): animals were infected by subcutaneous route with 150 bloodstream trypomastigotes of T cruzi Y strain; Group 3 -Immunized Group (AdASP-2): animals were immunized by intramuscular injection (im) route with 50 µL of AdSP-2 (2 × 10 8 plaque forming units [pfu]/cam) at day 0; Group 4-Immunized and Infected Group (AdASP-2 +TC): animals were immunized by im route with 50 µL of ASP-2 (2 × 10 8 pfu/ cam) and infected by T cruzi at the same day (day 0). It was observed a significant decrease of nests in the group that was immunized with AdASP-2 and infected on the same day. Tumor necrosis factor alpha (TNF-α) and inducible nitric oxide synthase (iNOS) gene expressions showed a significant increase in the AdASP-2 +TC group when compared to TC group, but it was noted that Cyclooxygenase-2 (Cox-2) was increased in TC group when compared to AdASP-2+TC group. Increase of matrix metalloproteinases-2 (MMP-2) and decrease of MMP-9 immunoexpression in the AdASP-2+TC group was noticed as well. Oxidative DNA damage was present in myocardium for AdASP-2+TC group as a result of 8-hydroxydeoxyguanosine immunoexpression. Taken together, our results highlighted an increased oxidative stress, MMP-2 activity and inflammatory host response promoted by AdASP-2 against T cruzi infection. K E Y W O R D S amastigote surface protein-2 (ASP-2), cardiomyocyte, gene expression, histopathology, Trypanosoma cruzi (T cruzi), vaccine J Cell Biochem. 2019;120:3373-3383.wileyonlinelibrary.com/journal/jcb

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Protective effects of purple carrot extract (Daucus carota) against rat tongue carcinogenesis induced by 4-nitroquinoline 1-oxide

Cited by 20 publications

References 57 publications

Synergistic Therapeutic Effect of Honokiol and 5-Fluorouracil on the Induced-Tongue Cancer in Rats.

Synergistic Therapeutic Effect of Honokiol and 5-Fluorouracil on the Induced-Tongue Cancer in Rats.

Stress hormones promote DNA damage in human oral keratinocytes

Therapeutical effects of vaccine from Trypanosoma cruzi amastigote surface protein 2 by simultaneous inoculation with live parasites

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