Dietary habits of men from Podlasie region of Poland in the years 1987-1998 analysed with self-organizing neural networks.

The study was conducted on a group of 556 men. Their dietary habits were evaluated 3 times in the years 1987-1998 by the frequency of consumption of 41 food items during last three months. Obtained frequencies were processed by self-organizing Kohonen neural network, allowing to group persons of similar dietary habits into 3 clusters. After analysing frequencies of consumption of each food item in each cluster, in view of health value, one model was described as appropriate, while remaining were described as two different inappropriate models. In three studies during 11 years, statistically significant increase in frequency of appropriate model was observed. That increase was linked with decrease of occurrence of inappropriate models. Additional verification of described models revealed significant differences between them in nutritive ingredients intake, and also in concentrations of HDL cholesterol in the blood serum of men assigned to those dietary patterns.

The diminution of liver glutathione content and changes in activities of antioxidant enzymes in long-term acetaldehyde poisoning.

The effect of acetaldehyde administration for 4 weeks on antioxidant protection systems was investigated in liver of rats. Liver SOD activity was decreased from control value 542.4 U/g of tissue to 411.2 U/g of tissue in experimental group (24% decrease). GSH-Px activity was practically unchanged and liver CAT activity was significantly decreased (35%). Sulfhydryl compounds in liver non-proteins following ACH treatment were decreased from 4.22 mumol/g of tissue in control group to 2.86 mumol/g of tissue (23%). Furthermore acetaldehyde treatment caused significant increase in MDA level in liver (78% increase).

The decrease of superoxide dismutase activity and depletion of sulfhydryl compounds in ethanol-induced liver injury.

There appears to be increasing evidence that ethanol toxicity may be associated with an increased production of reactive oxygen intermediates. In rats we studied the effect of 4 weeks of ethanol ingestion on the liver cytosolic defense system against active oxygen species. Compared with the control rats, the ethanol-fed animals had a significantly higher liver malondialdehyde content and significantly lower reduced glutathione level. Moreover, ethanol feeding resulted in a decrease of superoxide dismutase and catalase activities while glutathione peroxidase activity was only slightly diminished. Thus, prolonged ethanol administration profoundly modified the hepatic status of the enzymatic defense system leading to lipid peroxidation that may disrupt vital functions of liver cells.

The effect of immunostimulatory drugs on sulfhydryl compounds in plasma, liver and brain after ethanol-induced liver injury in rats.

Sulfhydryl compounds in plasma, liver and brain of rats treated with two immunostimulant drugs, isoprinosine and levamisole, after alcoholic liver injury have been investigated. After use of both drugs for 6 days we found partially beneficial effect on the SH-groups in plasma and liver. No changes in nonprotein SH compounds were observed in rat brain after treatment with isoprinosine, levamisole or ethanol. Furthermore, levamisole shortens the time necessary for the return of AlAT activity to normal value.

Studies on the kinetics of Na+/H+ exchange in OK cells: introduction of a new device for the analysis of polarized transport in cultured epithelia.

The present study describes a new perfusion technique--based on the use of a routine spectrofluorometer--which enables fluorometric evaluation of polarity, regulation and kinetics of Na+/H+ exchange at the level of an intact monolayer. Na+/H+ exchange was evaluated in bicarbonate-free solutions in OK (opossum kidney) cells, a renal epithelial cell line. Na+/H+ exchange activity was measured by monitoring changes in intracellular pH (pHi) after an acid load, using the pH-sensitive dye 2'7'-bis (carboxyethyl) 5-6-carboxy-fluorescein (BCECF). Initial experiments indicated that OK cells grown on a permeable support had access to apical and basolateral perfusion media. They also demonstrate that OK cells express an apical pHi recovery mechanism, which is Na+ dependent, ethylisopropylamiloride (EIPA) sensitive and regulated by PTH. Compared to resting conditions (pHi = 7.68; pHo = 7.4) where Na+/H+ exchange is not detectable, transport rate increased as pHi decreased. A positive cooperativity characterized the interaction of internal H+ with the exchanger, and suggests multiple H+ binding sites. In contrast, extracellular [Na+] increased transport with simple Michaelis-Menten kinetics. The apparent affinity of the exchanger for Na+ was 19 mM at an intracellular pH of 7.1 and 60 mM at an intracellular pH of 6.6. Inhibition of Na+/H+ exchange activity by EIPA was competitive with respect to extracellular [Na+] and the Ki was 3.4 microM. In conclusion, the technique used in the present study is well suited for determination of mechanisms involved in control of epithelial cell pHi and processes associated with their polarized expression and regulation.

The effect of Heparegen and D-penicillamine on the activity of some ammonia metabolizing enzymes in liver and brain of rats intoxicated with ethanol.

This paper reports data on the effect of two drugs: Heparegen (thiazalidine-4-carboxylic acid) and D-penicillamine on the blood ammonia concentration and on some ammonia metabolizing enzymes in liver and brain of rats intoxicated with ethanol. It seems, that both drugs decrease ammonia concentration and simultaneously elevate liver and brain glutamine synthetase activity. The effect of D-penicillamine on the nitrogen metabolism in the damaged liver appears to be more favorable than that of Heparegen.

[Effect of pesticides on selected biochemical parameters in the serum and liver of rats]. / Wplyw pestycydów na wybrane parametry biochemiczne w surowicy i watrobie u szczurów.

The experiments were carried out on male Wistar rats, weighing 200-250 g. The animals received oil or oily solutions of carbaryl, parathion-methyl and IPO62 in doses of 0.5, 0.1 or 0.02 LD50. 1, 2, 4 or 24 h after the administration of pesticides, the activities of ChE and blood glucose level, liver glycogen level, FFA and TG concentrations in serum and TG level in liver were estimated. Comparing the enzymatic changes in acute intoxications with carbaryl, parathion-methyl or IPO62, in the same doses, it was found that mechanisms of efficacy of those compounds had different trends. Changes in the activities of such parameters as ChE in serum, BGR, AspAT and AlAT in serum and liver and blood glucose level depend on the dose of pesticides and this effect is observed for IPO62, parathion-methyl and carbaryl.

Branched-chain amino acid enriched diet given simultaneously with ethanol partially prevents morphological and biochemical changes in the liver.

Morphological examination of the liver and biochemical studies of the serum were carried out on rats fed: a) ethanol p.o. in the daily dose of 6 g/kg for 4 weeks and maintained on standard diet (Et-OH) and b) ethanol in the same doses but fed the BCAA enriched diet (to amount of 1.174 mM/day/rat) were carried out. It can be concluded that BCAA enriched diet given simultaneously with ethanol prevent in part the morphological and ultrastructural changes in liver and improve positive body weight gain of experimental animals.

Ethanol decreases the level of sulfhydryl compounds in red blood cells and changes their hematological pattern in rats.

The level of sulfhydryl compounds in red blood cells (RBCs) and plasma and some haematological parameters were investigated in rats treated with ethanol for 4 weeks (daily dose of 6g/kg, 30% w/v, p.o.). After ethanol ingestion, the significant decrease of non-protein - SH groups were observed in RBCs and plasma. In treated rats, the mean corpuscular haemoglobin concentration (MCHC) was decreased and the mean corpuscular volume (MCV) was increased. There is a positive correlation between these two parameters and decreased content of sulfohydryl groups in RBCs.

Prostaglandin blockade blunts the natriuresis of elevated renal interstitial hydrostatic pressure.

Previous studies have shown that renal interstitial volume expansion (RIVE) increases renal interstitial hydrostatic pressure and urinary sodium excretion. In the present study we investigated whether blockade of prostaglandin synthesis inhibits the increase in fractional sodium excretion induced by RIVE. Expansion of the renal interstitial volume was achieved by injecting 50 microliters of 2.5% albumin solution into a polyethylene matrix chronically implanted in the left kidney. Fractional sodium excretion (FENa), renal interstitial hydrostatic pressure (PI), and urinary prostaglandin excretion (UPGE2) were measured before and after RIVE in eight control, seven meclofenamate-treated, and eight indomethacin-treated rats. RIVE in the control animals resulted in significant increases in PI (delta + 4.2 +/- 0.8 mmHg), in FENa (delta + 1.02 +/- 0.27%), and in UPGE2 (% delta + 150 +/- 38%) without significant changes in glomerular filtration rate. Inhibition of prostaglandin synthesis with meclofenamate or indomethacin attenuated the natriuretic response and blocked the increase in UPGE2 associated with RIVE. In summary, direct increases in renal interstitial hydrostatic pressure increase UPGE2 and urinary sodium excretion. This natriuretic response is markedly diminished by inhibition of prostaglandin synthesis. These studies suggest that prostaglandin synthesis may have an important role in mediating the natriuretic effect of increased renal interstitial hydrostatic pressure during renal interstitial volume expansion.

Effect of direct increases in renal interstitial hydrostatic pressure on sodium excretion.

This study examined the effect of increases in renal interstitial hydrostatic pressure (PI) on sodium excretion (UNaV) utilizing a direct technique for increasing renal interstitial volume. PI was increased by renal interstitial volume expansion (RIVE) via injection of 50 microliters of a 2% albumin in saline solution into the renal interstitium through a chronically implanted interstitial catheter. RIVE resulted in a stable increase in PI (4.6 +/- 0.4 to 9.4 +/- 0.8 mmHg) that was sustained over a 30- to 40-min period without significant changes in renal blood flow or glomerular filtration rate. Increases in PI were associated with significant increases in urine flow (13.8 +/- 3.4 to 31.7 +/- 5.0 microliters/min) and UNaV (2.3 +/- 0.6 to 6.2 +/- 1.1 micro eq/min) and fractional excretion of Na (2.6 +/- 0.8 to 6.9 +/- 1.5%). To determine the importance of albumin in maintaining an elevated PI, the effects of renal interstitial injections of saline were compared with albumin in saline solution. Injection of 50 microliters of saline into the renal interstitium had no sustained effect on PI. Injection of 2% albumin in saline solution in the same group of rats resulted in significant elevations in PI and UNaV. These data indicate that direct increases in PI via renal interstitial volume expansion result in significant increases in UNaV, thus supporting a role for PI in controlling UNaV.

The effect of methylbromophenvinfos (Polfos) on some enzymes in vivo and in vitro. I. In vivo studies.

The experiment was carried out on Wistar rats receiving orally either oil or oily solution of methylbromophenvinfos (Polfos) either in a single dose of 0.5 LD50, or doses of 0.1 LD50 once daily for a period of 2, 4 or 6 weeks. The activities of cholinesterase (ChE), beta-glucuronidase (beta-glu), lipase and amylase were assayed in the blood serum, the activity of acetylcholinesterase (AChE)-in brain homogenates, and the activities of lipase and amylase-in homogenates of the pancreas. Cholinesterases were inhibited in the course of both acute and chronic poisoning with Polfos. During the acute poisoning a sharp increase in the activity of beta-glu in the blood serum, 1 and 2 h after the pesticide administration, was observed. Polfos inhibited lipase and amylase both after acute and chronic treatment.

Effects of adenosine infusion into renal interstitium on renal hemodynamics.

This study was designed to investigate the hemodynamic effects of exogenous adenosine in the interstitium of the rat kidney. Adenosine or its analogues were infused into the renal interstitium by means of chronically implanted capsules. Infusion of adenosine (bolus 0.5 mumol plus 0.1 mumol/min) decreased glomerular filtration rate (GFR) from 0.81 +/- 0.06 (mean +/- SE) to 0.37 +/- 0.06 ml/min while having no effect on renal blood flow (RBF). The metabolically stable analogue, 2-chloradenosine (2-ClAdo), (bolus 10 nmol plus 2 nmol/min) decreased GFR from 0.73 +/- 0.07 to 0.21 +/- 0.06 ml/min. Interstitial infusion of theophylline, an adenosine receptor antagonist, completely abolished the effects of adenosine and 2-ClAdo on GFR. The distribution of adenosine, when infused into the renal interstitium, was determined using radiolabeled 5'-(N-ethyl)-carboxamidoadenosine (NECA), a metabolically stable adenosine agonist. After continuous infusion, [3H]NECA was distributed throughout the kidney. The effects of NECA to reduce GFR were similar to those of adenosine and 2-ClAdo. We conclude that increased levels of adenosine in the renal interstitium markedly decrease GFR without affecting RBF in steady-state conditions. The marked effects of adenosine agonists during their infusion into the renal interstitium and the complete blockade of these effects by theophylline suggest an extracellular action of adenosine.

Parathion-methyl effect on the activity of hydrolytic enzymes after single physical exercise in rats.

Rats were subjected to physical exercise in the form of a single race in a treadmill. Unexercised animals and those immediately or 1 h after the exercise were given oil or oily solution of parathion-methyl in a dose of 10 mg/kg by stomach gauge. At 1 h after pesticide administration the activity of cholinesterase (ChE) was determined in the serum, of paraoxonase--in the serum and liver, and that of beta-glucuronidase (beta-gluc)--in the serum, liver and intestine. Single physical exercise increased ChE activity in the serum, inhibited paraoxonase activity in the serum and liver; on the other hand, it did not affect significantly beta-gluc activity in the serum, but inhibited that enzyme in a transient manner in the liver and activated it in the intestine. In acute poisoning with parathion-methyl it was observed that ChE and paraoxonase activities were inhibited, while beta-gluc activity was enhanced in the serum. Single physical exercise either diminished or had no effect on enzymatic changes observed in acute poisoning with parathion-methyl.

The effect of chronic physical exercise on the activity of hydrolytic enzymes in acute poisoning with parathion-methyl in rats.

Parathion-methyl, 10 mg/kg p.o., was given to unexercised rats, rats trained for 3 weeks and resting for 2 days, and trained rats subjected to a single physical exercise before treatment. The activity of cholinesterase (ChE) in the serum, of paraoxonase--in the serum and liver, and of beta-glucuronidase (beta-gluc)--in the serum, liver and intestine were determined 1 h after the treatment. Repeated physical exercise increased beta-gluc activity in the serum and liver and inhibited it in the intestine, while a single race after repeated exercise inhibited paraoxonase activity in the serum. Parathion-methyl inhibited ChE and paraoxonase activities and an increased beta-gluc activity in the serum. Repeated physical exercise and a single race, applied 2 days after the end of training, affects the activity of parathion-methyl in a significant yet diversified manner, dependent upon the examined biochemical parameters.

Blood glucose and insulin concentration in rats subjected to physical exercise in acute poisoning with parathion-methyl.

Unexercised rats or those subjected to single physical exercise were given parathion-methyl (10 mg/kg p.o. - 0.5 DL50) or oil (vehicle). Blood glucose and serum insulin concentration were assayed 1 h after the treatment. Physical exercise depressed the serum insulin concentration without changes in blood glucose level. In acute poisoning with parathion-methyl hyperglycemia occurred concurrently with hypoinsulinemia. Physical exercise abolished the pesticide-induced hypoinsulinemia, but not hyperglycemia.

Effect of lithium on renal gluconeogenesis.

Lithium at a concentration of 5 mM reduced by half gluconeogenesis from di- and tricarboxylic substrates, and abolished the activating effect of dibutyryl-cAMP in the isolated rat kidney cortex tubules. The effect of lithium and ouabain on renal gluconeogenesis is additive. Similarly as by lithium, glucose synthesis is inhibited at higher pH values and increased concentration of bicarbonates. Inhibition of gluconeogenesis by lithium is most probably due to the inhibition of the luminal transport of dicarboxylic substrates into the kidney cell and lowered intracellular metabolism, resulting probably from the increased cytoplasmic pH and bicarbonate concentration.