Nutrient intake and influence on markers of oxidative stress in zoo managed male snow leopards (Uncia uncia)

Oxidative stress (OS) results from overproduction of reactive species. Nutrient intake can contribute positively or negatively to OS and lack of established nutrient requirements for most exotic species managed in zoos exacerbates possibilities for nutrient imbalances that potentially could lead to reactive species production. The objective of this study was to evaluate the influence of nutrient intake and nutritional husbandry on markers of OS in male snow leopards (n = 14) maintained in U.S. facilities (n = 12). Diet samples and husbandry information were obtained and snow leopards were immobilized once for collection of blood. Samples were analyzed for chemical composition (diet and blood), antioxidant capacity (blood), and markers of OS (blood). Correlations between weekly nutrient intakes and markers of OS were analyzed by linear regression. Analyzed markers of OS included antioxidant enzymes (superoxide dismutase (SOD) and glutathione peroxidase (GPx)) and ferric reducing antioxidant potential (FRAP) that are protective against OS, and protein carbonyls (PC), thiobarbituric acid reactive substances (TBARS), and DNA/RNA damage that are indicative of oxidative damage. Weekly copper intake (10.1 – 80.2 mg) was negatively correlated with DNA/RNA damage (R 2 = 0.44; P = 0.01). Weekly sodium intake (4.4 – 12.7 g) was positively correlated with GPx activity (R 2 = 0.43; P = 0.04). More frequent feeding of whole prey (0.3 – 3 times/wk) was correlated with increased blood SOD activity (R 2 = 0.55; P < 0.01). In conclusion, greater dietary copper intake and more frequent feeding of whole prey may reduce OS in snow leopards. Dietary sodium intake and relationship with GPx activity should be further evaluated to determine benefit or detriment. No cause and effect can be inferred from our results, but our data suggest altering dietary form and nutrient concentrations may influence OS in snow leopards.

Beneficial Effects of Glucagon-Like Peptide-1 (GLP-1) in Diabetes-Induced Retinal Abnormalities: Involvement of Oxidative Stress

Background: Hyperglycemia-induced oxidative stress plays a key role in diabetic complications, including diabetic retinopathy. The main goal of this study was to assess whether the topical administration (eye drops) of glucagon-like peptide-1 (GLP-1) has any effect on oxidative stress in the retina. Methods: db/db mice were treated with eye drops of GLP-1 or vehicle for three weeks, with db/+ mice being used as control. Studies included the assessment by western blot of the antioxidant defense markers CuZnSOD, MnSOD, glutathione peroxidase and reductase; immunofluorescence measurements of DNA/RNA damage, nitro tyrosine and Ki67 and Babam2 proteins. Results: GLP-1 eye drops protected from oxidative stress by increasing the protein levels of glutathione reductase, glutathione peroxidase and CuZnSOD and MnSOD in diabetic retinas. This was associated with a significant reduction of DNA/RNA damage and the activation of proteins involved in DNA repair in the retina (Babam2) and Ki67 (a biomarker of cell proliferation). Conclusions: GLP-1 modulates the antioxidant defense system in the diabetic retina and has a neuroprotective action favoring DNA repair and neuron cells proliferation.

Beneficial Regulation of Cellular Oxidative Stress Effects, and Expression of Inflammatory, Angiogenic, and the Extracellular Matrix Remodeling Proteins by 1α,25-Dihydroxyvitamin D3 in a Melanoma Cell Line

The causes of cancer include the cellular accumulation reactive oxygen species (ROS), which overrides the cellular antioxidants such as superoxide dismutase, from intrinsic aging, genetics, and exposure to environmental pollutants and ultraviolet (UV) radiation. The ROS damage biomolecules such as DNA (including p53 gene), RNA, and lipids, and activate inflammatory, angiogenic, and extracellular matrix (ECM) remodeling proteins; which collectively facilitate carcinogenesis. The 1α,25-dihydroxyvitamin D3 (Vitamin D) has anti-carcinogenic potential from its antioxidant, anti-inflammatory, and endocrine properties. We examined the anti-carcinogenic mechanism of vitamin D through the beneficial regulation of oxidative stress effects (oxidative DNA/RNA damage, superoxide dismutase expression, membrane damage, and p53 promoter activity), and expression (at the protein, mRNA and/or promoter levels) of inflammatory mediators (interleukin-1 (IL-1) and tumor necrosis factor-α (TNF-α)), angiogenic mediators (transforming growth factor-β (TGF-β), and vascular endothelial growth factor (VEGF)), and the ECM remodeling proteins (matrix metalloproteinases (MMP)-1 and MMP-2) by vitamin D in melanoma cells. Vitamin D inhibited oxidative DNA/RNA damage and membrane damage; and stimulated superoxide dismutase expression and p53 promoter activity in melanoma cells. It inhibited the expression of IL-1, TNF-α, TGF-β, VEGF, MMP-1 and MMP-2 by transcriptional or post-transcriptional mechanisms. We conclude that vitamin D is beneficial to melanoma cells through the inhibition of oxidative DNA/RNA damage, membrane damage, and the expression of inflammatory, angiogenic and ECM remodeling proteins; and the stimulation of superoxide dismutase expression and p53 promoter activity.