Publications by authors named "S C Kivatinitz"

The objective of the present research was to evaluate commercially available milk powders according to their protein oxidative modifications and antioxidant capacity, and to evaluate if these characteristics are related to physical quality parameters such as dispersibility or stability during storage. Fifteen commercially processed spray-dried milk powders were evaluated: 6 whole milk powders (WMP), 4 skim milk powders (SMP), and 5 infant formula powders (IFP). Protein oxidative status was measured as protein carbonyl (PC) content, dityrosine content, and extent of protein polymerization.

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We investigated how protein changes occur, at the primary or higher structural levels, when proteins are exposed to UV or fluorescent (FL) light while in the complex matrix, milk. Whole milk (WM) or skim milk (SM) samples were exposed to FL or UV light from 0 to 24h at 4°C. Protein oxidation was evaluated by the formation of protein carbonyls (PC), dityrosine bond (DiTyr), and changes in molecular weight (protein fragmentation and polymerization).

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We developed a simple microtechnique to measure lipids in milk by UV spectrophotometry. This technique is based upon the property of fatty acids to absorb UV light proportional to their concentration. Samples of powdered or fluid milk (30 or 60 muL) were added to 3 mL of analytic grade ethanol and stored at -20 degrees C for at least 1 h.

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In this study, we tested the antiproliferative effects of mannan from Aloe saponaria using normal murine (SpMC) and human cells (PBMC) and several tumoral cell lines. Employing flow cytometry, it could be determined that mannan inhibits the proliferative response in normal and tumoral cells. Mannan affects the expression of CD3(+) SpMC indicating that mannan inhibits mainly T lymphocyte proliferative response.

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Human very-low-density lipoprotein (VLDL) inhibits DNA synthesis in lymphocytes activated by the nonspecific mitogen concanavalin A (Con A). We studied the effects of VLDL on lymphocyte activation (IL-2 receptor expression), cell cycle progression, and production of IL-2 and of IL-4 (a proinflammatory and an anti-inflammatory interleukin, respectively) to understand why an atherogenic lipoprotein inhibits cell proliferation. After 48 h of stimulation with the mitogen, VLDL decreased the population of cells bearing IL-2 receptor and the population of T-cells that progress through the cell cycle, increasing the population of T-cells in G(0)/G(1).

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