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Biomedical subjects

S E Kays

Publications and source records attributed to S E Kays.

9 recordsLinked to original sources
PubMed2000

Determination of total dietary fiber of intact cereal food products by near-infrared reflectance.

Near-infrared reflectance spectra of cereal food products were acquired with a commercial dual-diode-array (Si, InGaAs) spectrometer customized to allow rapid acquisition of scans of intact breakfast cereals, snack foods, whole grains, and milled products. Substantial gains in the performance of multivariate calibration models generated from these data were obtained by a computational strategy that systematically analyzed the performance of various spectral windows. The calibration model based on 137 cereal food products determined the total dietary fiber (TDF) content of a test set of 45 intact diverse cereal food products with root-mean-squared error of cross-validation of between 1.8 and 2.0% TDF, relative to the laborious enzymatic-gravimetric reference method. The calibration performance is adequate to estimate TDF over the range of values found in diverse types of cereal food products (0.7-50.1%). The method requires no sample preparation and is relatively unaffected by specimen moisture content.

Calibration↗
PubMed1996

Transforming growth factor-beta 1 inhibits regeneration of renal proximal tubular cells after oxidant exposure.

Transforming growth factor-beta (TGF-beta), a regulatory cytokine expressed in the kidney, plays a role in nephrogenic repair. This study utilized a chemical model of renal proximal tubule cellular injury and regeneration to investigate the effects of TGF-beta 1 on regeneration. Confluent monolayers of rabbit renal proximal tubular cells (RPTC) in primary culture exposed to the oxidant t-butylhydroperoxide (800 microM TBHP) for 1.5 hours were 24% confluent after 24 hours. Confluency increased to 50% 4 days after TBHP exposure. Recovery of monolayer confluency was associated with increased monolayer protein but not with DNA content. Daily treatment of injured monolayers with TGF-beta 1 inhibited the recovery of monolayer confluency and inhibited recovery of protein content in a concentration-dependent manner (0.02-1 ng/mL). DNA content of injured monolayers was not altered by TGF-beta 1. A single treatment of injured monolayers with 0.2 ng/mL (8 pM) TGF-beta 1 inhibited recovery of monolayer confluency and protein content without altering monolayer DNA content. These data show that a single 24 hour exposure to a low concentration (8 pM) of TGF-beta 1 inhibits regeneration of renal proximal tubule cell monolayers following oxidative injury by inhibiting, in part, cellular migration/spreading.

Animals↗
PubMed1995

Regeneration of renal proximal tubule cells in primary culture following toxicant injury: response to growth factors.

Growth factors may play an important role in the repair of the renal proximal tubule epithelium following toxic injury. This study investigated the regeneration of rabbit renal proximal tubule cell (RPTC) monolayers following exposure to the nephrotoxicants tert-butylhydroperoxide (TBHP) and 1,2-dichlorovinyl-L-cysteine (DCVC), and the effect of exogenous growth factors on the regeneration process. Confluent monolayers exposed to TBHP or DCVC for 1.5-2 hr were 23 and 43% confluent, respectively, after 24 hr. Confluency increased to 63 and 80% 4 days after TBHP or DCVC exposure, but decreased to 29 and 24% after 8 days. Monolayer DNA content did not increase after TBHP or DCVC exposure; however, monolayer protein/DNA ratio increased above control values after DCVC exposure. Recovery of confluency was not sensitive to RGD-containing peptides that inhibit the binding of integrins to extracellular matrix. Epidermal growth factor (EGF) treatment resulted in complete recovery of confluency, and protein and DNA contents 4-6 days after injury. Unlike EGF, IGF-1 or insulin treatment produced a small increase in confluency following TBHP exposure. These results suggest that hypertrophy following DCVC exposure and migration/spreading after TBHP and DCVC exposure play a partial and temporary role in the regeneration of RPTC monolayers, that in the absence of exogenous growth factors proliferation and complete regeneration of the monolayer does not occur, that toxicants may alter the production of mitogenic factors, and that EGF is a potent and efficacious growth factor in promoting regeneration.

Animals↗
PubMed1993

An in vitro model of renal proximal tubule cell regeneration.

The ability of renal cells to regenerate is critical for the recovery of renal function following injury. Research on the recovery of renal function has been limited by the lack of in vitro models of renal repair. The goal of this study was to develop an in vitro model of renal proximal tubule cell (RPTC) injury and regeneration using primary cultures of rabbit RPTC. Renal proximal tubules were isolated and cultured in hormonally defined DME/F-12 medium at 37 degrees C under 95% air/5% CO2. RPTC were grown to confluency, made quiescent by the removal of insulin and hydrocortisone from the medium for 24-48 hr, and treated with the nephrotoxicant, 1,2-dichlorovinyl-L-cysteine (DCVC). DCVC (100 microM for 2 hr, n = 3-6) resulted in cell injury and the release of nonviable cells from the plate at 24 hr (55% +/- 6% confluency, mean +/- SEM) and 48 hr (37% +/- 7% confluency). Cell monolayers began to regenerate 96 hr after exposure (57% +/- 9% confluency) and continued to regenerate reaching 76% +/- 8% and 84% +/- 1% confluency by 6 and 8 days postexposure. Control cells maintained confluency throughout the experiment. Thus, an in vitro primary cell culture model has been developed in which the cell monolayer regenerates after nephrotoxicant-induced injury. This model may be useful in the study of mechanisms of renal cell injury and repair.

Animals↗
PubMed1992

Cephaloridine nephrotoxicity is potentiated by selenium deficiency but not copper deficiency in rats.

Lipid peroxidation may contribute to the nephrotoxicity of cephaloridine, a beta-lactam antibiotic. Copper and Se may protect against free radical damage, and dietary Se deficiency potentiates cephaloridine nephrotoxicity. The objectives of this study were to further investigate potentiation of cephaloridine toxicity by Se deficiency and to determine whether Cu deficiency increases cephaloridine-induced injury. Weanling male Sprague-Dawley rats were fed adequate, Cu-deficient, Se-deficient, and Se and Cu-deficient diets for 4 wk and subsequently injected i.p. with cephaloridine (1200 mg/kg body wt) or saline. Nephrotoxic response to cephaloridine occurred, with increased plasma urea, kidney weight, excretion of urinary enzymes, and kidney lesions. Cephaloridine also increased plasma sorbitol dehydrogenase activity. Selenium deficiency depressed kidney glutathione peroxidase activity (78%) and potentiated cephaloridine nephrotoxicity. Copper deficiency did not increase cephaloridine nephrotoxicity; the small depression (13%) in kidney Cu,Zn-superoxide dismutase activity may not have been sufficient to impair antioxidant status. However, the marked depression in kidney glutathione peroxidase activity during Se deficiency may have impaired antioxidant status and enhanced cephaloridine-induced injury. In contrast to results in the kidney, neither Se deficiency nor Cu deficiency potentiated cephaloridine hepatotoxicity, as assessed by plasma SDH activity.

Animals↗
PubMed1991

Iron supplementation increases gentamicin nephrotoxicity in rats.

Gentamicin (GM), an aminoglycoside antibiotic, can cause acute renal failure in humans and experimental animals. It has been proposed that lipid peroxidation may play a role in GM nephrotoxicity. Nutrients such as copper, selenium or iron that influence lipid peroxidation may also be a factor in toxicity. This study investigated the effect of supplemental dietary iron on the nephrotoxicity of GM. Weanling male Sprague-Dawley rats were fed control [0.75 mmol (42 mg) iron/kg] or iron-supplemented [4.32 mmol (242 mg) iron/kg] diets for 3 wk. Rats were subsequently injected intraperitoneally with GM (50 or 100 mg.kg body wt-1.d-1) or saline for 8 d. High dietary iron resulted in greater sensitivity to GM (100 mg/kg body wt) toxicity in terms of elevated urinary excretion of n-acetyl-beta-glucosaminidase (NAG) and increased mineralization, casts and megalocytes in renal tubules. After GM treatment was terminated, NAG excretion decreased with both dietary treatments. However, renal tubular cell damage, due to GM, remained higher than in saline-treated controls in rats fed 4.32 mmol iron/kg diet.

Acute Kidney Injury↗
PubMed1990

Influence of copper nutrition on gentamicin nephrotoxicity in rats.

Lipid peroxidation may play a role in the acute nephrotoxicity of gentamicin (GM). Copper (Cu) depletion is associated with reduced activity of certain antioxidant enzymes in tissues, and with kidney lesions and impaired renal function. This study, therefore, investigated the effect of Cu nutrition on GM nephrotoxicity. Weanling male Sprague-Dawley rats were fed Cu adequate or Cu depleted diets for 16 days, then injected intraperitoneally with GM (0-100 mg.kg body weight-1.day-1) for 8 days. GM, but not mild Cu depletion, induced lesions in the kidney and increased plasma urea and urinary excretion of n-acetyl-beta-glucosaminidase. Lower iron in Cu-depleted kidneys and normal Cu, Zn-superoxide dismutase may have prevented additional GM damage during mild Cu depletion.

Animals↗
PubMed1971

Enhancement of Nitrate Reductase Activity by Benzyladenine in Agrostemma githago.

Nitrate reductase activity in excised embryos of Agrostemma githago increases in response to both NO(3) (-) and cytokinins. We asked the question whether cytokinins affected nitrate reductase activity directly or through NO(3) (-), either by amplifying the effect of low endogenous NO(3) (-) levels, or by making NO(3) (-) available for induction from a metabolically inactive compartment. Nitrate reductase activity was enhanced on the average by 50% after 1 hour of benzyladenine treatment. In some experiments, the cytokinin response was detectable as early as 30 minutes after addition of benzyladenine. Nitrate reductase activity increased linearly for 4 hours and began to decay 13 hours after start of the hormone treatment. When embryos were incubated in solutions containing mixtures of NO(3) (-) and benzyladenine, additive responses were obtained. The effects of NO(3) (-) and benzyladenine were counteracted by abscisic acid. The increase in nitrate reductase activity was inhibited at lower abscisic acid concentrations in embryos which were induced with NO(3) (-), as compared to embryos treated with benzyladenine. Casein hydrolysate inhibited the development of nitrate reductase activity. The response to NO(3) (-) was more susceptible to inhibition by casein hydrolysate than the response to the hormone. When NO(3) (-) and benzyladenine were withdrawn from the medium after maximal enhancement of nitrate reductase activity, the level of the enzyme decreased rapidly. Nitrate reductase activity increasd again as a result of a second treatment with benzyladenine but not with NO(3) (-). At the time of the second exposure to benzyladenine, no NO(3) (-) was detectable in extracts of Agrostemma embryos. This is taken as evidence that cytokinins enhance nitrate reductase activity directly and not through induction by NO(3) (-).

Journal Article↗