Green Synthesized Zinc Oxide Nanoparticles as Feed Additives to Improve Growth, Biochemical, and Hematological Parameters in Freshwater Fish Labeo rohita.

Zinc deficiency in aquatic animals affects the biological processes and physiological functions. Thus, the supplement of ZnONPs can be used as an alternative method to overcome zinc deficiency. Nanoparticles have the potential to enhance the growth and health of the fish. The main aim of this study is to evaluate the growth efficacy of ZnONP-supplemented diet with fingerlings of Labeo rohita. The green synthesized ZnONPs were characterized by ultraviolet-visible (UV-Vis) spectroscopy, Fourier transformer infrared spectroscopy (FTIR), X-ray diffraction (XRD), scanning electron microscopy (SEM), and energy dispersive spectroscopy (EDS). Different concentrations of ZnONPs (5, 7.5, and 10 mg/kg) were administered in the basal diet of freshwater fish Labeo rohita for 45 days to observe the growth and metabolic functions of the body. However, the fish fed with 10 mg/kg ZnONP-supplemented diet shows that the growth performance was highly increased followed by 7.5 mg/kg and 5 mg/kg ZnONPs when compared with the control. The biochemical, hematological, and digestive enzyme activities were also significantly increased with different concentrations of ZnONPs. The effects of zinc oxide nanoparticles show the higher improvement of growth and metabolic functions in Labeo rohita. These results suggest that the nanotechnology could apply for feed formulation technology and pave the way for the dietary supplementation of zinc oxide nanoparticles as safe ingredients for aquatic animals to overcome the zinc deficiency.

Epigallocatechin gallate supplementation protects against renal injury induced by fluoride intoxication in rats: Role of Nrf2/HO-1 signaling.

Fluoride intoxication generates free radicals, causing oxidative stress that plays a critical role in the progression of nephropathy. In the present study, we hypothesized that epigallocatechin gallate (EGCG), found in green tea, protects the kidneys of rats treated with fluoride by preventing oxidative stress, inflammation, and apoptosis. Pretreatment of fluoride-treated rats with EGCG resulted in a significant normalization of creatinine clearance and levels of urea, uric acid, and creatinine. Fluoride intoxication significantly increased renal oxidative stress markers and decreased the levels of renal enzymatic and non-enzymatic antioxidants. In addition, renal NO, TNF-α, IL-6 and NF-κB were also increased in the renal tissue of fluoride-treated rats. Further, EGCG pretreatment produced a significant improvement in renal antioxidant status and reduced lipid peroxidation, protein carbonylation and the levels of inflammatory markers in fluoride-treated kidney. Similarly, mRNA and protein analyses showed that EGCG pretreatment normalized the renal expression of Nrf2/Keap1 and its downstream regulatory proteins in fluoride-treated rat kidney. EGCG also effectively attenuated fluoride-induced renal apoptosis by the up-regulation of anti-apoptotic proteins such as Bcl-2 and down-regulation of Bax, caspase-3, caspase-9 and cytochrome c. Histology and immunohistochemical observations of Kim-1 provided further evidence that EGCG effectively protects the kidney from fluoride-mediated oxidative damage. These results suggest that EGCG ameliorates fluoride-induced oxidative renal injury by activation of the Nrf2/HO-1 pathway.