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Results for “AMMONIUM CHLORIDE”

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PubMed1997

The effect of ammonium chloride on hepatic and renal metabolism in the rat.

The metabolic effects of an ammonium salt on the liver and kidney were investigated. Rats were allowed free access to a 0.28 M ammonium chloride (NH4Cl) solution for 7- and 8-day periods. Serum urea concentration was significantly increased after 8 days of NH4Cl ingestion. However the following hepatic urea cycle enzymes remained unchanged: CPS, OTC, ASS and ASL. The pattern of urinary urea excretion was variable. When the data for the 7-day period were pooled, there was no significant difference between the control and acidotic groups. However, when they were examined on a daily basis, acidosis significantly decreased urea excretion on day 2. Urea excretion then began to increase, reached the control value on day 4 and was significantly greater than the control value on day 7. Urinary ammonium excretion of the acidotic group was significantly increased on day 2 and continued to rise throughout the 7-day period. Renal phosphate-dependent glutaminase of the acidotic group was significantly increased on the eighth day. These data indicate that NH4Cl ingestion alters the pattern of urea excretion in a manner not previously demonstrated.

Acidosis↗
PubMed1973

Algicidal activity of a surface-bonded organosilicon quaternary ammonium chloride.

The hydrolysis product of a quaternary amine-containing organosilicon salt, 3-(trimethoxysilyl)-propyldimethyloctadecyl ammonium chloride, was found to exhibit algicidal activity while chemically bonded to a variety of substrates. Six representative species of Chlorophyta, Cyanophyta, and Chrysophyta were used to evaluate the algicidal activity. Substrate-bonded (14)C-labeled organosilicon quaternary ammonium salt when attached to nonwoven fibers was durable to repeated washings, and algicidal activity could not be attributed to slow release of the chemical.

Ammonium Chloride↗
PubMed2004

Prevention of hydrogen peroxide-induced apoptosis of human peripheral T cells by a lysosomotropic iron chelator, ammonium chloride.

Human peripheral T cells are considered to be easily susceptible to oxidative stress because these cells lack peroxidase activity. Therefore, in a previous study, we investigated the site of ROS formation by utilizing Mito-Capture, H(2)DCFDA (succinimidyl ester of dichlorodihydrofluorescein diacetate), DAPI (4',6-diamidino-2-phenylindole), and LysoSensor. Our results showed that ROS formation was apparently diffusely distributed in T cells oxidatively stressed with 0.1 mM hydrogen peroxide. Moreover, lysosomal swelling and deformity, possibly revealing lysosomal membrane destabilization, were observed in these cells. Based on the above-mentioned results, we concluded that an apoptotic cascade involving early lysosomal membrane destabilization exists in the hydrogen peroxide-induced apoptosis of human peripheral T cells. Therefore, the possible involvement of lysosomal protease leakage caused by hydroxyl radical formation in lysosomes (possibly resulting in mitochondrial membrane dysfunction) is considered to play an important role in hydrogen peroxide-induced T cell apoptosis. Hydrogen peroxide-mediated destabilization of lysosomal membranes with release of hydrolytic enzymes such as many kinds of cathepsins into the cell cytoplasm can lead to a cascade eventuating in cell death. To assess the importance of the intralysosomal pool of redox-active iron, we examined the effect of blockade of lysosomal digestion by exposing T cells to the lysosomotropic alkalinizing agent ammonium chloride (NH(4)Cl). Preincubation of human peripheral T cells with 10 mM NH(4)Cl for 4 h dramatically decreased apoptotic death caused by subsequent exposure to hydrogen peroxide (H(2)O(2)), and lysosomes and mitochondria showed almost normally preserved appearance. Therefore, we concluded here that lysosomal protease leakage caused by hydrogen peroxide in T cells was prevented by preincubation with ammonium chloride (NH(4)Cl).

Ammonium Chloride↗
PubMed1989

Effect of ammonium chloride on the bicarbonate buffer system in heat-stressed broilers.

1. The effects of ammonium chloride (NH4Cl) on the bicarbonate buffer system and plasma lactate in heat-stressed broilers were investigated. 2. The infusion of a 10 g/l solution of NH4Cl into the crop during a 90 min thermoneutral period produced a metabolic acidosis resulting from a reduction in blood bicarbonate concentration. Blood bicarbonate continued to decrease in NH4Cl-treated birds and reached values which were 30% of controls by the end of a 90 min heat stress period. 3. By the end of heat stress, plasma lactate concentrations were lower in NH4Cl-infused birds than in controls.

Acid-Base Equilibrium↗
PubMed2001

Effect of ammonium chloride on Biomphalaria alexandrina and on its infection with Schistosoma mansoni and Echinostoma liei miracidia.

Ammonium chloride (NH4Cl) has molluscicidal activity against B. alexandrina. The LC50 and LC90 recorded of this salt were found to be 90 ppm and 130 ppm, respectively. Maintaining of B. alexandrina at low concentrations of NH4Cl (5, 10, 15 and 20 ppm) greatly reduced their survival rate and fecundity. The net reproductive rate (Ro) [sigmaIx Mx] was deleteriously affected. This rate was significantly reduced than that of control snails in all tested snail groups. The reduction in Ro was 86.9%, 90.8%, 93.9% and 96.9%, respectively. The susceptibility of B. alexandrina to infection with S. mansoni and E. liei miracidia and infectivity of these two parasites were greatly reduced. Increasing the salt concentration increased this reduction. The magnitude of reduction in infection rate was lower in case of E. liei than that in S. mansoni indicating that E. liei is more tolerant to the effect of this salt than S. mansoni.

Ammonium Chloride↗
PubMed1986

Occupational dermatitis to 2,3-epoxypropyl trimethyl ammonium chloride.

4 workers developed hand dermatitis in an automated starch modification process plant. 2,3-epoxypropyl trimethyl ammonium chloride (EPTMAC), a quaternary ammonium compound used as a cationizing chemical, produced allergic reactions in all 4 patients. They had only been in contact with EPTMAC for a short time before developing dermatitis, which indicates that EPTMAC is a strong sensitizer. Immunohistochemistry and electron microscopy showed the features of an allergic patch test. An industrial hygiene project was initiated at the factory to prevent new cases. It revealed many risks of skin contact with the process chemicals. Thus an automated process does not guarantee protection.

Allergens↗
PubMed1989

The effect of chronic dietary acidification using ammonium chloride on acid-base and mineral metabolism in the adult cat.

Adult cats with normal renal function were fed a nutritionally balanced, vitamin A-replete, experimental dry diet with or without ammonium chloride (NH4Cl) for 6 mo to study the effects of chronic dietary acidification on acid-base parameters and the metabolism of selected minerals. Dietary balance studies were performed monthly. Blood and urine samples were collected monthly to evaluate acid-base parameters, plasma parathyroid hormone (PTH) and 1.25-dihydroxycholecalciferol levels. Ammonium chloride-treated cats had significantly lower blood and urinary pH, and lower blood bicarbonate concentrations. Treated cats also had higher blood ionized calcium concentrations, hypercalciuria and lower intestinal calcium absorption relative to baseline (prior to feeding the experimental diet) and to control cats. This resulted in the development of lower calcium balance in the first several months. PTH levels were unaffected by dietary acidification; however, 1.25-dihydroxycholecalciferol levels were significantly decreased in treated cats. Treated cats had negative potassium balance during 5 mo of dietary acidification. Magnesium, sodium, and phosphorus balances were lower, but positive, in treated cats compared to control cats. Cats consuming the NH4Cl-supplemented diet had increased chloride balance. Thus, chronic dietary acidification with 1.5% NH4Cl produced chronic metabolic acidosis and lower or negative, calcium and potassium balance.

Acid-Base Equilibrium↗