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Objectives: The current research explores the anticancer effects of pH sensitive CVC-ZnO QDs (Carvacrol-loaded Zinc Oxide Quantum Dots) on DMBA induced mammary carcinoma in rats. Methods: Female SD rats were used, and mammary cancer was induced by chemical carcinogen via subcutaneous injection near the mammary gland. Different concentrations of CVC-ZnO QDs were orally supplemented to evaluate the optimum dose. We assessed the growth rate, body weight changes, tumor volume, tumor incidence and tumor burden in both the inducer and treatment groups. We also evaluated the biochemical parameters (antioxidant status, lipid peroxidation, detoxification enzymes, and lipid profile) and histopathological changes in the kidney and mammary tissues. Results: Our findings indicate that CVC-ZnO QDs treated rats significantly decreased the tumor weight, incidence, burden, lipid peroxidation levels, phase I detoxification enzyme activities and increased the body weight, phase II detoxification enzyme activities, and antioxidant status compared to the DMBA alone treated rats. CVC-ZnO QDs treatment also altered the lipid profile of plasma and mammary tissue. Furthermore, histopathological results confirmed that the CVC-ZnO QDs protect against DMBA-mediated damage to the mammary and kidney. Conclusion: The findings indicate that the CVC-ZnO QDs administered at 4 mg/kg b.w exhibited a significant anticancer effect against DMBA-induced mammary cancer.

The structural integrity and excellent immune system of the skin makes it a protective covering, inspite of its exposure to hazardous compounds. In the present study, the chemopreventive efficacy of D-carvone was studied in 7, 12-dimethylbenz[a]anthracene (DMBA) induced skin carcinogenesis. DMBA (25 μg in 0.1 m L−1acetone) was used to induce skin cancer in Swiss albino mice. Animals were randomly divided into six groups of six animals in each. Different concentrations of D-carvone (10, 20, 30 mg/kg body weight) were used to assess its anticancer effect. Tumor incidence, tumor volume, tumor burden, histological examination and levels of phase I and phase II detoxification agents were analyzed in experimental animals. Further, expression of p53 and various apoptotic proteins including- Bcl-2, Bax was analyzed using immunohistochemistry and enzymatic expression of apoptotic proteins caspase-3 and caspase-9 was carried out by using ELISA. We observed 100% tumor incidence in DMBA-painted animals and our results showed that D-carvone at 20 mg dose significantly prevents skin carcinogenesis. Our results also showed decreased levels of phase I enzymes (Cyt P450 and-Cyt b5) with increased levels of phase II enzymes (GR, GST and GSH) and increased expression of Bax, caspase-3 and caspase-9 with decreased expression of mutated p53 and Bcl-2 in animals treated with DMBA and D-carvone at 20 mg dose. The results of the present study suggest that D-carvone can be used as a chemopreventive agent against skin cancer, as it induces apoptosis in cancer. However, further studies are warranted to check chemopreventive efficacy of D-carvone on cell proliferation, angiogenesis, and metastasis before going to human trial.

The effect of silibinin on lipid profile, colonic mucin content, transforming growth factor beta (TGF-β) expression, cell proliferation and apoptosis in high fat diet fed rats challenged with 1, 2 dimethyl hydrazine (DMH) was investigated. Rats were randomized into six groups. Group 1: Control rats; Group 2: Silibinin (50 mg/kg of b.w. p.o every day); Group 3: DMH (20 mg/kg b.w.); Groups 4–6: DMH + Silibinin (Initiation, Post-initiation and entire period treatment regimens, respectively). At the end of 32nd week, DMH alone administered rats showed hyperlipidaemia and colon tumour burden with decreased mucin content. The expression of TGF-β was found to be lost in the early adenoma but increased stromal positivity of TGF-β was observed in adenocarcinoma of the colon. Evasion of apoptosis is also seen in the colon of tumour bearing rats. These DMH induced pathological changes were attenuated by silibinin supplementation reflecting its antihyperlipidaemic, colon protective and anticarcinogenic effects.

Background: Zirconium Oxide (ZrO2) is one of the most widely used metal oxide nanoparticles with unique features that permit its usage in various medical applications, including drug delivery, targeting, labelling, and loading. Rutin is a bioflavonoid found in various natural sources and has diverse biological activities and pharmaceutical applications. Some studies have evaluated the impacts of ZrO2 NPs on aquatic creatures, but little is known about their ability to recover after exposure. Since the toxicity of ZrO2 nanoparticles is not known, it would be crucial to investigate their toxicity using zebrafish (Danio rerio) as a model organism. Objectives: In the present work, the toxicity of ZrO2 was investigated in Danio rerio using behavioural alterations, biomarkers of oxidative stress and cellular damage. The morphology of the gill tissues, as well as the optimal amount of rutin for mitigating deleterious effects was evaluated. Materials and Methods: Fish were treated for 14 days, and seven study groups were examined: control, ZrO2 exposure alone at three distinct concentrations (5 mg/L, 10 mg/L, and 20 mg/L), and combined with rutin (100 mg/L). Results: Compared to control groups, Danio rerio treated with ZrO2 alone or in combination with rutin produced worse outcomes. However, rutin-supplemented groups exhibited greater improvement than ZrO2 alone groups. ZrO2 affects cells by causing oxidative stress and decreasing the antioxidants SOD, CAT, GPx, GSH, and Vitamin C. Enhanced oxidative stress induces behavioural and morphological modifications. The structural examination of the gill tissues revealed hyperplasia, lamellar fusion, filament erosion, and a dilated marginal channel or epithelial lifting. Conclusion: According to our data, the sub-lethal concentration of ZrO2 NPs for Danio rerio is 10 mg/L. Although ZrO2 was detrimental to the groups exposed to it, supplementing 100 mg/L of rutin was able to protect against its toxicity. [ABSTRACT FROM AUTHOR]