Showing papers on "7,12-Dimethylbenz[a]anthracene published in 2020"
TL;DR: The CX3CL1-CX3CR1 axis can crucially contribute to skin carcinogenesis by regulating the accumulation and functions of TAMs and can be a good target for preventing and/or treating skin cancers.
21 citations
TL;DR: These findings indicate that single cell RNA-seq can help reveal the dynamics of molecular signaling pathways for porcine oocytes treated by DMBA, and supplement of anti-oxidative reagents could not sufficiently rescue DMBA-induced defects of porcina oocytes.
8 citations
TL;DR: It is suggested that CYP1A, CYP3A, and GST enzyme activities participate in the protective mechanism of morin against endosulfan and DMBA induced toxicity.
Abstract: Morin is a flavonoid which is present in many plants. Endosulfan and 7,12-dimethylbenz[a]anthracene (DMBA) are toxic chemicals that humans are exposed to in their daily lives. In this study, the pr...
8 citations
TL;DR: Hsperetin exhibits the potential protective effect against DMBA-induced oral cancer through apoptotic and anti-proliferative properties, however, a long-term observation would be needed to confirm the possibility of malignant change of the resulted dysplastic lesions upon he Speretin pretreatment.
Abstract: Oral squamous cell carcinoma (OSCC) is widespread malignant neoplasm and refractory cancers in worldwide. Here, we studied the chemopreventive potential of hesperetin on 7,12-dimethylbenz(a)anthrac...
6 citations
TL;DR: The results suggest that anti-estrogenic and anti-proliferative effect of AITC prevent the development of DMBA and MNU-induced mammary carcinogenesis in rat.
Abstract: The anti-estrogenic and anti-cell proliferative effect of allyl isothiocyanate (AITC) was carried out by analyzing the status of sex hormones and its receptors and cell proliferative markers in chemically induced mammary carcinogenesis in rats. Mammary tumor was induced by a single dose of DMBA (25 mg/rat) and MNU (50 mg/kg bw) injected subcutaneously near mammary gland. RT-PCR, western blotting and immunohistochemical analysis of mammary tissues show an upregulation of ER-α, PR, aromatase, PCNA, cyclin D1 and AgNORs staining and down regulation of p53 expression as well as plasma estradiol, prolactin and testosterone levels increased in DMBA and MNU-induced tumor bearing rats. Oral administration of AITC at a dose of 20 mg/kg bw restored the levels of sex hormones and its receptors, aromatase, cell proliferative markers and AgNORs staining near to normal levels. Molecular docking studies also supported these findings. The results suggest that anti-estrogenic and anti-proliferative effect of AITC prevent the development of DMBA and MNU-induced mammary carcinogenesis in rat.
5 citations
TL;DR: Daucosterol showed for the first time in vivo antitumor effects that corroborate its previous in vitro effects.
Abstract: This study aimed to evaluate the in vivo anticancer effects of daucosterol which was earlier reported to possess in vitro anticancer effects. Breast tumor was induced in 30 rats using the environmental carcinogen 7,12-dimethylbenz(a)anthracene (DMBA) while 6 control rats received olive oil (NOR). Animals with palpable tumors were randomized into five groups (n = 6) each as follows: negative control group treated with the vehicle (DMBA); positive control group treated with 5 mg/kg BW doxorubicin (DOXO + DMBA); three groups treated with daucosterol at doses of 2.5, 5, and 10 mg/kg BW (DAU + DMBA). Treatment lasted 28 days afterward, tumor (mass, volume, cancer antigen [CA] 15-3 level and histoarchitecture), hematological and toxicological parameters were examined. The tumor volume gradually increased in the DMBA group during the 28 days, with a tumor volume gain of ∼390 cm3 . Daucosterol at all doses reduced tumor volume (∼133.7 cm3 at 10 mg/kg) as well as protein, malondialdehyde (MDA), and CA 15-3 levels compared to DMBA rats. Tumor sections in daucosterol-treated rats showed a lower proliferation of mammary ducts with mild (5 and 10 mg/kg) to moderate (2.5 mg/kg) inflammatory responses. Moreover, it exhibited an antioxidant effect, evidenced by a significant and dose-dependent decreased in MDA levels, as well as an increase in catalase activity compared to the DMBA group. Daucosterol showed for the first time in vivo antitumor effects that corroborate its previous in vitro effects.
5 citations
TL;DR: It is suggested that NOB has an anticell proliferative effect on DMBA-induced mammary cancer via modulation of the AP-1 signaling pathway.
Abstract: Breast cancer is a widespread disease that affects women globally. Diagnostic processes and remedial approaches to breast carcinogenesis have improved in recent decades, but continuous survival of patients with breast carcinogenesis is still lacking due to increased cell proliferation. The aim of the present work is to explore the anticell proliferative effects of nobiletin (NOB) against 7,12-dimethylbenz[a]anthracene (DMBA)-treated mammary tumorigenesis in rats. We stimulate mammary carcinogenesis using oral gavage of DMBA (25 mg/kg body weight) mixed with olive oil (1 mL). This results in reduced body weight; increased liver marker enzymes such as alkaline phosphatase, acid phosphatase, aspartate aminotransferase, and alanine aminotransferase; and cell proliferative markers such as c-Jun, proliferating cell nuclear antigen, c-Fos, cyclin D1, and activating protein-1 (AP-1) in the DMBA-treated cancer-bearing animals. NOB administration improved body weight, significantly reduced hepatic marker enzymes, and altered histopathological changes. Furthermore, NOB efficiently reduced tumor cell proliferation markers in DMBA-induced mammary carcinogenesis. Overall, these results suggest that NOB has an anticell proliferative effect on DMBA-induced mammary cancer via modulation of the AP-1 signaling pathway.
4 citations
TL;DR: Empirical and experimental studies indicate that high consumption of vegetables helps to lower risk of breast cancer, and genetic, environmental, and lifestyle factors interacting to cause this disease.
3 citations
TL;DR: It is concluded that β‐elemene prevents DMBA/TPA promoted skin carcinogenesis through its antioxidant and abate inflammation markers and cell‐proliferative markers also activating proapoptotic molecules.
Abstract: β-Elemene (1-methyl-1-vinyl-2,4-diisopropenyl-cyclohexane), a natural sesquiterpene-derived curcumae radix, exhibits a variety of pharmacologic properties including anticancer. However, the molecular action of β-elemene in chemical-induced skin carcinogenesis remains unclear. Therefore, the present study executes to investigate a possible effect of β-elemene in the 7,12-dimethylbenz(a)anthracene (DMBA)/12-O-tetradecanoylphorbol-13-acetate (TPA)-promoted skin tumor model. The experimental mice were subjected to execute two-stage skin carcinogenesis and it has been initiated by the addition of DMBA on the dorsal portion of the mouse skin. One week after, for chemical carcinogen of mice, topical exposure of DMBA has been induced following with TPA (5 nmol) in acetone (200 μL) given weekly twice for 20 weeks respectively. After completion of the experimental period, we noticed that 100% of tumor incidence, histopathological changes, decreased lipid peroxidation (LPO), and decreased antioxidant levels in DMBA/TPA-promoted skin carcinogenesis. Furthermore, enhanced activity of inflammatory protein markers (nuclear factor [NF]-κB, tumor necrosis factor-α, interleukin-6, cyclooxygenase-2, and nitric oxide synthase) and cell-proliferative messenger RNA markers (PCNA, cyclin D1), and increased antiapoptotic protein Bcl-2; decreased proapoptotic protein marker events Bax and caspase 3 and 9 expressions were noticed in DMBA/TPA promoted skin tissue. In this study, we noticed that β-elemene noticeably reversed the histopathological changes and antioxidant levels in tumor-bearing mice. Conversely, β-elemene effectively inhibits inflammation, cell proliferation events, and enhances proapoptotic factors, by suppression of NF-κB transcriptional activation in DMBA/TPA animals. Thus, we concluded that β-elemene prevents DMBA/TPA promoted skin carcinogenesis through its antioxidant and abate inflammation markers and cell-proliferative markers also activating proapoptotic molecules.
3 citations
22 Jan 2020
TL;DR: Hamsters scarified at 5 weeks and 10 weeks demonstrated mild and moderate dysplasia, respectively, and dimethylbenz(a)anthracene is a useful tool for inducing dysplastic lesions in the buccal pouch mucosa of hamsters.
Abstract: Induction of premalignant lesions in animal models is of high value for research purposes. This study aimed to induce dysplasia in hamster mucosal pouch for investigation of dysplastic lesions using dimethylbenz(a)anthracene. The buccal pouch of 10 hamsters was painted with dimethylbenz(a)anthracene for 10 weeks every other day. At 5 and 10 weeks, they underwent histopathological analysis. Clinically, there was no change until week 7; after which mucosal thickening occurred. Hamsters scarified at 5 weeks and 10 weeks demonstrated mild and moderate dysplasia, respectively. dimethylbenz(a)anthracene is a useful tool for inducing dysplastic lesions in the buccal pouch mucosa of hamsters.
2 citations
TL;DR: The findings suggest that CRE could be a potential agent useful in therapeutic approaches for curing the disease caused by aberrant cells.
Abstract: Background: The carcinogenic substance 7,12-Dimethylbenz[a]anthracene (DMBA) was commonly used to induce tumor formation in rodents. The development of tumor may trigger higher expression of pro-inflammatory cytokines, which in turn supports tumor progression. In this study, we examined the efficacy of Cyperus rotundus extract (CRE) that was reported to have anti-inflammatory properties. We focused on investigating the levels of activated T lymphocytes and the pro-inflammatory cytokines expressed by macrophages. Methods: Female BALB/c were injected with DMBA subcutaneously. The DMBA exposed mice were given CRE orally in three different doses; 63.33, 158.4, and 316.8 mg/kg. After 14 days, the levels of activated T lymphocytes and pro-inflammatory cytokines were analyzed using flow cytometry. Graphical analysis was done with FlowJo v10 and followed by statistical analysis. Results: The treatment of CRE reduced the population of CD4 and CD8 T cells. The number of activated CD4 and CD8 T cells were also significantly suppressed. The population of macrophages marked by CD11b cells was significantly reduced. Finally, the CRE treatment suppressed the levels of TNF-α, IFN-γ, IL-1β, and IL-6 expressed by macrophages. Conclusion: Our findings suggest that CRE could be a potential agent useful in therapeutic approaches for curing the disease caused by aberrant cells.
TL;DR: The present findings suggest that the tumour preventive effect of myrtenal could partly be ascribed to its apoptotic induction potential during DMBA induced oral carcinogenesis.
Abstract: Apoptotic avoidance is one of the foremost characteristic features of tumour cells. Apoptotic induction in cancer cells could thus help to identify new anticancer agents from the natural products. The present study has taken an effort to investigate the apoptotic efficacy of myrtenal, a monoterpene, in 7,12-dimethylbenz(a)anthracene (DMBA) induced oral carcinoma in male golden Syrian hamsters. The present study used the potent carcinogen, 7,12- dimethylbenz(a)anthracene, to develop oral tumours in the buccal pouches of the golden Syrian hamsters. Topical application of the above said carcinogen on the buccal mucosa (3 times a week for 14 weeks) resulted in well differentiated oral squamous cell carcinoma. The apoptotic potential of myrtenal was investigated using a spectrum of apoptotic markers, including pro-apoptotic and anti-apoptotic markers. Oral tumours developed in the buccal mucosa of hamsters showed higher expression of mutant p53 protein, Bcl-2 and lowered expression of Bax, Bad, Bid, caspase 3 and caspase 9. Myrtenal treatment at a dose of 230mg/kg bw orally to the hamsters treated with DMBA modulated the above said apoptotic markers towards tumour suppression or inhibition. The present findings thus suggests that the tumour preventive effect of myrtenal could partly be ascribed to its apoptotic induction potential during DMBA induced oral carcinogenesis.
08 May 2020
TL;DR: The administration of C. aeruginosa extract during and after carcinogen induction gave several impacts on rat carcinogenesis, with the highest dose found to cause changes in white pulp and marginalis zone boards indicating that it takes higher dose to cause an immune response effect reaching the organs.
Abstract: Present investigation shows that the extract of C. aeruginosa attenuates DMBA-induced spleen carcinogenesis in Wistar rats. Three-week female Wistar rats were treated with three different C. aeruginosa extract doses (CA1: 40 mg/200 g body weight, BW; CA2: 80 mg/200 g BW; CA3: 160 mg/200 g BW) and were induced with DMBA after one-week administration of these doses. A commercial immunostimulant, and DMBA only were also given to each group as positive and negative control, respectively. The development of tumors was evaluated by investigating the incidence of tumor and tumor multiplicity during the experiment. Spleen mass index and histological parameters such as white pulp, centrum germinativum, and marginalis zone were also examined. Based on our study, the administration of C. aeruginosa extract during and after carcinogen induction gave several impacts on rat carcinogenesis. At the extract dose of 80 mg/200 g BW, tumor incidence of animals were least (P<0.05). However, all doses did not show any effect to the spleen mass index, though the highest dose (160 mg/200 g BW) was found to cause changes in white pulp and marginalis zone boards. This trend indicates that it takes higher dose to cause an immune response effect reaching the organs.
TL;DR: The results resolved that sclareol has probably owing to its antioxidant or scavenging properties of free radical and transition act on phase I and II enzymes in regards to the evacuation of metabolites carcinogenesis, which is evoked by DMBA in hamster’s buccal pouch.
Abstract: Sclareol has demonstrated a broad variety of biological activities that belong to the antioxidant anti-inflammatory and anticancer activities that are used in traditional medicine. In the current study, we intended to explore the antitumor possible of sclareol along 7, 12-dimethylbenz (a) anthracene (DMBA) evoked golden Syrian hamster’s buccal pouch carcinogenesis. Lipid peroxidation and antioxidants were assessed by the buccal tissue, and plasma of DMBA evoked golden Syrian hamster buccal pouch carcinogenesis of observational animals. We observed 100% of tumor establishment and noted defects in the biochemical restrictions of lipid peroxidation and antioxidants and also histopathological observations of carcinogenesis in the hamster’s buccal pouch in DMBA only. Sclareol (20 mg/b.wt) has significantly inhibited the tumor burden, tumor volume, and increased phase II detoxification enzymes, antioxidant level, lipid peroxidation, and also phase I enzymes and has improved the histopathologically changes during carcinogenesis in the buccal pouch of DMBA induced golden Syrian hamster. The outcomes of the present scrutinized study proposed that aiming biochemically and histopathologically that act upon the inheritance of cancer characteristics is an effectual system for chemoprevention. Therefore, our results resolved that sclareol has probably owing to its antioxidant or scavenging properties of free radical and transition act on phase I and II enzymes in regards to the evacuation of metabolites carcinogenesis, which is evoked by DMBA in hamster’s buccal pouch.
TL;DR: Both ?
Abstract: Objective: ?-carrageenan is a food stabilizer agent which has an antiproliferative effect, while vitamin D is a prohormone acts on the nuclear receptor and has a cytotoxic against cancer. This study aimed to show the synergistic effect of using topical ?-carrageenan and oral administration of the vitamin D on the 7, 12-dimethylbenz[a] anthracene (DMBA)-induced oral cancer. Material and Methods: fifty four male albino rats were randomly divided into seven groups: Acetone-treated served as control (Group I), vitamin D (5000UI)-treated (Group II), ?-carrageenan (1%)- treated (Group III), DMBA (0.5%)-treated (Group IV), Acetone, ?-carrageenan and DMBA were administered topically on both cheeks and palate, five times weekly for 12 weeks, while the vitamin D was administered orally twice weekly for 12 weeks. Groups V, VI, and VII were animals treated with vitamin D, ?-carrageenan, and both vitamin D and ?-carrageenan for 8 weeks after induction of oral cancer. At the end of the study, blood samples were obtained by cardiac puncture for determination of TNF-? and EGFR. Results: In the groups III and IV, serum EGFR showed significant low levels compared with Group I. In the Group VII, serum EGFR showed a significantly (p=0.014) low level compared with Group IV (614.3±69.7 pg/ml versus 882.4±45.6 pg/ml, respectively). Higher percentages of high levels of TNF-? were observed in the Groups VI and VII, while a lower percentage of EGFR was observed in the Group VI. Conclusion: both ?-carrageenan and vitamin D have antiproliferative effect against DMBA-inducing oral cancer by increasing the levels of TNF-? and suppressing the signaling pathway of EGFR. Concomitant using ?-carrageenan and vitamin D reduces the antiproliferative effect of each other. KeywordsOral cancer; 7, 12-dimethylbenz[a] anthracene; Vitamin D; ?-carrageenan; Epidermal growth factor receptor; Tumor necrosis factor-?.
31 Mar 2020
TL;DR: Interestingly, it is found for the first time that topical application of ASC on the dorsal skin of DMBA-initiated and TPA-promoted mice significantly accelerated skin tumorigenesis and raised tumor multiplicity as compared to the positive control group (DMBA/TPA).
Abstract: Se-allylselenocysteine (ASC), an analogue of garlic bioactive compound, has been shown to inhibit mammary carcinogenesis in vivo and cell growth in vitro. However, the function of ASC on anti-inflammatory effects remains largely unknown. Therefore, we investigated whether ASC has an anti-inflammatory effect on lipopolysaccharide (LPS)-induced inflammation or an anti-tumor effect promoting on DMBA/TPA-induced skin tumorigenesis and tried to elucidate the mechanisms involved. Herein, the results showed that ASC inhibited LPS-induced production of nitric oxide (NO) with a decreased protein level of inducible nitric oxide synthase (iNOS) in RAW 264.7 cells. However, ASC enhanced LPS-induced cyclooxygenase-2 (COX-2) protein levels and mRNA expression. Interestingly, we found for the first time that topical application of ASC on the dorsal skin of DMBA-initiated and TPA-promoted mice significantly accelerated skin tumorigenesis and raised tumor multiplicity as compared to the positive control group (DMBA/TPA). The number of tumours that were 1–3, 3–5, and >5 mm in size per mouse increased in a dose-dependent manner in the ASC pre-treated groups. Pre-treatment with ASC showed a significant increase in the expression of COX-2 compared with the positive control group. Thus, ASC may modulate the COX-2 protein expression and promote DMBA/TPA-induced skin cancer in mice.
TL;DR: Proper balance between LPO and antioxidants should be maintained in the cell because of their potential importance in the pathogenesis of various pathologic diseases including cancer.
Abstract: In recent years, there has been a growing interest in studying the role played by lipid peroxidation (LPO) and antioxidant status. Proper balance between LPO and antioxidants should be maintained in the cell because of their potential importance in the pathogenesis of various pathologic diseases including cancer. Neoplastic cells may sequester essential antioxidants from circulation to supply the demands of growing tumor. Reactive oxygen species (ROS) are involved in the initiation and progression of carcinogenesis. Moreover, the ROS-induced oxidative damage causes a decrease in the efficiency of antioxidant defense mechanism (Padmavathi et al., 2006). Hence, oxidative International Journal of Current Microbiology and Applied Sciences ISSN: 2319-7706 Volume 9 Number 7 (2020) Journal homepage: http://www.ijcmas.com
TL;DR: The results showed that cecropin B has been able to reduce tumor growth and have little side effects on hematologic factors probably through apoptosis.
Abstract: Background and aims: Antimicrobial peptides constitute a family of bioactive peptides that are involved in the body defense. Recently, their anti-cancer properties, especially by inducing apoptosis, have been proven in in vitro studies. Therefore, in this study, the effects of cecropin B as an antimicrobial peptide on breast cancer growth, hematological parameters, and histopathological changes in rats were evaluated. Methods: Twenty-four female rats were randomly divided into 4 groups. The cancer group, control group, cecropin B group, and cancer group treated with cecropin B. The tumor size was measured at the beginning and the completion of the treatment period. Blood samples were collected for assessment of the hematological parameters and Bax and Bcl2 levels. Tumor tissues were removed for histopathological analysis. Results: The tumor size had a significant increase in the cancer group and cancer group treated with cecropin at the end of the treatment. A significant decrease in mean cell volume, white blood cell count and Bcl2 level and a significant increase in hemoglobin and Bax levels were observed in the cancer group treated with cecropin B compared to cancer group. Changes in other parameters were not significant. Histopathological study showed the invasion of mitotic cells to stromal and muscular tissues of the breast in the cancer group, while focal destruction of tissue and cell death were observed in the cancer group treated with cecropin B. Conclusion: The results showed that cecropin B has been able to reduce tumor growth and have little side effects on hematologic factors probably through apoptosis.