Evaluation of Developmental Toxicity and Oxidative Stress Caused by Zinc Oxide Nanoparticles in Zebra Fish Embryos/ Larvae.

Zinc oxide nanoparticles (ZnO NPs) are used in various fields, including biological ones. ZnO NPs are eventually disposed of in the environment where they may affect natural systems, and there is no international law to regulate their manufacture, usage, and disposal. Hence, this present study is carried out to synthesise a more non-toxic and bioactive ZnO NPs from the marine algae Sargassum polycystum. The ZnO NPs were biologically produced using the marine algae Sargassum polycystum. The dynamic light scattering result describes that synthesised particles' average size is about 100 nm in diameter. Transmission electron microscopy (TEM) analysis demonstrated the rod-like morphology of ZnO NPs. Fourier tranform-infrared spectroscopy (FT-IR) results revealed the presence of functional groups in ZnO NPs. The selected area electron diffraction (SAED) results strongly suggested the ZnO NPs crystallinity. ZnO NPs surface morphology and compositions were identified by scanning electron microscopy (SEM- EDX) values. To analyse the toxicity of synthesised nanoparticles, zebra fish larvae were used, which involved subjecting embryos to various ZnO NPs concentrations at 1 hpf and analysing the results at 96 hpf. The 60 and 80 ppm sub-lethal doses were chosen for further studies based on the LC50 (82.23 ppm). In the ZnO NPs-treated groups, a significant slowdown in pulse rate and a delay in hatching were seen, both of which impacted the embryonic processes. A teratogenic study revealed a dose-dependent increase in the incidence of developmental deformities in the treated groups. Along with increased oxidants and a corresponding reduction in antioxidant enzymes, Na+ K+-ATPase and AChE activity changes were seen in ZnO NPs-treated zebra fish larvae groups. The apoptosis process was increased in ZnO NPs-treated groups revealed by acridine orange staining. These results indicate that the green synthesis process cannot mitigate the oxidative stress induced by ZnO NPs on oxidative signalling.

Malvidin Abrogates Oxidative Stress and Inflammatory Mediators to Inhibit Solid and Ascitic Tumor Development in Mice.

The anticancer activity of malvidin was studied in Dalton's lymphoma ascites (DLA)-induced solid and ascitic tumor mice models. Malvidin is a natural compound belonging to the family of O-methylated anthocyanidin and plays a predominant role in regulating both short- and long-term cellular activities. Animals were injected with DLA cells (1.5 × 106 cells/animal) to induce solid and ascitic tumors. The administration of malvidin (5 mg/kg bw and 10 mg/kg bw) was carried out for 10 consecutive days from the day of tumor induction for both solid and ascitic tumors. Cyclophosphamide, CTX (25 mg/kg bw), used as the standard drug, was also administered for 10 consecutive days. Treatment with malvidin showed a significant reduction in tumor volume and elevated white blood cell (WBC) count when compared to the DLA-bearing control animals. The treatment also maintained the body weight and hemoglobin level, and decreases in aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), gamma-glutamyl transferase (GGT) were also noted. This investigation also reported the decreased levels of cellular glutathione (GSH) in ascitic tumor groups. Malvidin reduced inflammatory mediator and cytokine levels, such as tumor necrosis factor level alpha (TNF-α) and interleukin-6 (IL-6), which serve as molecular targets for cancer prevention. A decrease in the level of reactive oxygen species (ROS), like nitric oxide (NO), was observed. Histopathological examination revealed altered morphological changes in tumor tissue and the alleviation of hepatic architecture due to DLA. Immunohistochemical analysis revealed the inhibition of iNOS. This study demonstrated that malvidin exhibited significant in vivo antitumor activity and that it was reasonably imputable to its increasing endogenous mechanism. We accent the pertinence of malvidin as a potential naturally derived drug target for tumor control.

In Vivo Anticancer Activity of Biosynthesized Zinc Oxide Nanoparticle using Turbinaria conoides on a Dalton's Lymphoma Ascites Mice Model.

In the present study, we aimed to evaluate the anticancer effect of zinc oxide nanoparticles (ZnO-NPs) synthesized from Turbinaria conoides against a murine model of Dalton's lymphoma ascites (DLA). Nanoparticles were synthesized from the hydroethanolic extract of T. conoides (HETC). An ultraviolet-visible spectrophotometric analysis was performed to confirm the formation of ZnO-NPs. Size, morphology, and elemental composition of ZnO-NPs were also analyzed using scanning electron microscopy-energy dispersive X-ray diffraction (SEM-EDX). Healthy Swiss albino mice were intraperitoneally induced with DLA cells and treated with ZnO-NPs and HETC at a dose of 50 µg/kg (p.o.). The effects of ZnO-NPs and HETC on body weight, tumor volume, hematological profile, and liver biochemical parameters were studied. The results of in vivo studies revealed that the treatment with ZnO-NPs and HETC decreased the tumor volume, thereby increasing the lifespan of DLA-bearing mice. The treatment also restored the alterations in hematological profile, antioxidant status, and activities of liver marker enzymes. These histopathological results provided the evidence for the protective effect of ZnO-NPs and HETC on DLA-induced mice. Thus, we conclude that ZnO-NPs possess more significant anticancer and antioxidant activities in DLA-bearing mice than HETC.