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The recent temperature extremes and other associated climatic events pose a detrimental effect to ruminant livestock. To abate this, it is necessary to adopt a functional (biotechnology) approach like the use of nano minerals as feed additives for normal immune function. Nano zinc oxide (nZnO) has demonstrated growth-promoting properties and has been reported to improve antioxidant capacities with high bioavailability recorded in ruminant. This study therefore aimed to research into nano zinc supplementation on growth performance, haematology, serum, oxidative and antioxidant enzymes of West African dwarf (WAD) goats. A total of 18 yearling WAD goats (7.2 ± 0.54 kg) were allocated into 3 treatments of 6 animals per treatment on weight equalization bases. Each group was randomly allotted to three (0, 300 and 600 mg/kg nZnO) experimental diets. Data on haematological parameters, serum minerals and serum biochemical parameters were collected on day 0 and day 84 of the experiment. Data collected were subjected to analysis of variance in a completely randomized design (CRD), and significant means were separated using Tukey's test. It was revealed that West African dwarf goats fed 600 mg/kg nZnO recorded the highest (p < 0.05) PCV and white blood cell values (32.00% and 5.70 × 103/L, respectively) while goats fed 300 mg/kg nZnO recorded the lowest values. At day 84, nZnO supplementation increased serum total protein, globulin and total cholesterol concentration, with higher values (7.57 g/dl, 4.17 g/dl and 95.73 mg/dl) recorded for goats fed 300 mg/kg nZnO. Lower aspartate aminotransferase (66.33 U/L) was observed for goats fed diets containing 300 g/kg nano zinc oxide. Serum minerals (phosphorus, zinc, copper and iron) were elevated in 600 mg/kg nZnO group. Supplementation of nZnO had no significant (p > 0.05) effect on blood superoxide dismutase (SOD) and total bilirubin concentration while reduced (p < 0.05) malondialdehyde (MDA) and urea values were recorded in 300 and 600 mg/kg nZnO supplemented treatments. Goats fed 600 mg/kg nZnO recorded a lower (p < 0.05) glutathione peroxidase value for kidney (24.78 U/mg) and forelimb cut (24.89 U/mg) while kidney, liver and forelimb cut SOD values (4.61, 2.45 and 5.84 U/mg, respectively) were highest at 300 mg/kg nZnO group. The study concluded that supplemented nZnO aided maintenance of and improved the health of the experimental animals through elevated PCV, serum parameters, reduced MDA, urea and other oxidative biomarkers in both serum and organs of West African dwarf goats. [ABSTRACT FROM AUTHOR]

Purpose: To measure the serum levels of the oxidative stress markers superoxide dismutase (SOD), malondialdehyde (MDA), and glutathione peroxidase (GPx) and compare them before and after zinc supplementation in patients with early age-related macular degeneration (AMD). Methods: We measured serum zinc levels in 65 patients with early AMD. Of these, 29 patients with macular drusen and a serum zinc level <80 μg/dL received oral zinc acetate dihydrate (50 mg/day). Serum trace metal levels (zinc and copper) and oxidative stress marker levels (SOD, MDA, and GPx) were measured at baseline and 12 weeks after the treatment. The macular drusen areas and best-corrected visual acuity were evaluated in 24 participants who attended the 3-month follow-up. Results: MDA level was significantly decreased from baseline to 12 weeks after zinc administration (170.5 ± 100.9 vs. 148.3 ± 57.9 pmol/mL, P = 0.03), while SOD was significantly increased from baseline to 12 weeks after zinc intake (4.2 ± 0.9 vs. 4.6 ± 0.9 U/mL, P = 0.03). The serum zinc level was significantly correlated with the MDA level (P = 0.03, ρ = -0.26). The area of soft drusen was significantly decreased after zinc treatment (1,936,654.9 ± 1,348,267.6 vs. 966,883.9 ± 719,938.1 μmm2, P = 0.04). Conclusions: The levels of oxidative stress markers MDA and SOD decreased and increased, respectively, after oral zinc administration to 24 patients with AMD. The therapeutic effect of zinc treatment on drusen area might differ depending on the drusen phenotype in early AMD. [ABSTRACT FROM AUTHOR]