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PubMed1965

[Analytical study of anticholinergics from the group of carboxylic acid esters. VI. Study of the stability of the chloride of the beta-diethylaminoethylester of diphenylhydroxyacetic acid (benactyzine), of the chloride of the beta-diethylaminoethylester of the phenyl-n-propylacetic acid (prospasmine), of the 2-(phenylcyclohexylhydroxyacetoxy)-ethyl-dimethyldulfonium iodide (hydroxythiospasmine) and of the 2-(phenylcyclohexylacetoxy)-ethyldimethylsulfonium iodide (thiospasmine)].

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Benactyzine↗
PubMedDate not supplied

Effects of cobalt chloride, nickel chloride, and nickel subsulfide upon erythropoiesis in rats.

The erythropoietic effects of sustained intraperitoneal (i.p.) administration of CoCl2 and NiCl2 were compared with the effects of a single intrarenal (i.r.) injection of alpha Ni3S2 in female Fischer-344 rats. Infusion of NiCl2 by osmotic minipumps (0.85 mg Ni per day, i.p., for 24 days; total dose = 20 mg Ni per rat) did not alter the blood hematocrit or reticulocyte count during six weeks of observation. Under identical conditions, i.p. infusion of CoCl2 (0.85 mg Co per day, i.p., for 24 days; total dose = 20 mg Co per rat) caused significant erythrocytosis (hematocrit at six weeks = 62 +/- 4 percent, P less than 0.001 versus 50 +/- 3 percent in controls) and reticulocytosis (reticulocyte count at three weeks = 2.5 +/- 1.5 percent, P less than 0.005 versus 0.8 +/- 0.7 percent in controls). Administration of alpha Ni3S2 to rats as a single i.r. injection (7 mg Ni per rat) caused pronounced erythrocytosis (hematocrit at six weeks = 79 +/- 2 percent, P less than 0.001 versus controls) and reticulocytosis (reticulocyte count at three weeks = 2.8 +/- 1.2 percent, P less than 0.005 versus controls). This study demonstrates that i.p. infusion of Ni[II] is ineffective in stimulating erythropoiesis in rats, and that salient differences exist between the enhanced erythropoiesis that occurs in rats following i.p. infusion of Co[II] and that produced by i.r. injection of alpha Ni3S2.

Animals↗
PubMed1993

The contact allergens nickel chloride and cobalt chloride directly induce expression of endothelial adhesion molecules.

Activation of vascular endothelium is a key event in the initial phase of an inflammatory reaction e.g. to contact allergens. In the present study the effect of two common contact sensitizers, NiCl2 and CoCl2, on endothelial expression of intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), and endothelial leukocyte adhesion molecule-1 (ELAM-1, E-selectin) was studied. NiCl2 and CoCl2 were found to upregulate these adhesion molecules on human umbilical vein endothelial cells (HUVEC) in a dose- and time-dependent manner as could be demonstrated by flow cytometry and enzyme-linked immunosorbent assay. During organ culture of foreskin samples treatment with NiCl2 led to upregulation of ELAM-1 and ICAM-1 but not VCAM-1 on microvascular endothelium. Induction of adhesion molecules by NiCl2 was found to depend on de novo mRNA and protein synthesis and could be blocked by the protein kinase inhibitor H-7 in a dose-dependent manner but not by HA-1004 and staurosporine. An autocrine IL-1-dependent mechanism mediating NiCl2 effects could be excluded. Our data demonstrate that allergens as NiCl2 and CoCl2 are capable of directly activating endothelium which is an important step in evolving inflammatory reactions and may thus be of relevance for the pathogenesis of contact hypersensitivity.

Allergens↗
PubMed1975

Chloride transport in human red cells.

1. The chloride equilibrium flux (chloride self-exchange) was determined by measuring the rate of 36Cl efflux from radioactively labelled human red cells. The cellular chloride concentration was varied between 5 and 700 mM by the nystatin technique (Cass & Dalmark, 1973). The chloride transport capacity was not affected by the nystatin technique. 2. The chloride equilibrium flux showed saturation kinetics in the pH range between 6-2 and 9-2 (0 degrees C). The chloride transport decreased at chloride concentrations higher than those which gave the maximum transport. 3. The apparent half-saturation constant, (K1/2), depended on the pH and whether the chloride transport was perceived as a function of the chloride concentration in the medium or in the cell water. The (K1/2)m increased and the (K1/2)c decreased with increasing pH. The dependence of the chloride transport on the chloride concentration was described by Michaelis-Menten kinetics at pH 7-2, but at values of pH outside pH 7-8 S-shaped or steeper graphs were observed. 4. The chloride equilibrium flux varied with the pH at constant chloride concentration in the medium (pH 5-7-9-5). The transport had a bell-shaped pH dependence at chloride concentrations below 200 mM. At chloride concentrations between 300 and 600 mM the chloride transport increased with increasing pH to reach a plateau around pH 8. The position of the acidic branches of the pH graphs was independent of the chloride concentration (25-600 mM), but the position of the alkaline branches moved towards higher values of pH with increasing chloride concentration (5-150 mM). Thus, the position of the pH optimum increased with increasing chloride concentration. The chloride transport at low pH values was a function of the inverse second power of the hydrogen ion concentration. The pK of the groups which caused the inhibition was approximately 6 and independent of the temperature (0-18 degrees C). 5. The chloride equilibrium flux as a function of chloride concentration, pH, and temperature could be described by a transport model with a mobile, positively charged, chloride binding carrier with a single chloride dissociation constant of 33 mM, a transport capacity of 900 m-mole/3 x 10(13) cells.min (pH 7-2, 0 degrees C), and an Arrhenius activation energy of 30 kcal/mole. The pH dependence of the transport of inorganic monovalent and divalent anions is discussed in relation to the suggested model.

Biological Transport↗
PubMed2004

[Anti-endotoxin effect of lanthanum chloride in vivo: an experimental study of mice].

OBJECTIVE: Lanthanum is one of rare earth with extremely active chemical property and has been evidenced to possess antibacterial effect as well as the function of blocking calcium flux and regulating cellular immunity. Our previous studies showed that lanthanum could affect the biological activity of LPS and inhibit the activity in vitro. In this study, we explored the anti-LPS effects of lanthanum chloride in vivo so as to provide evidence in searching for new anti-endotoxic agents for the prevention and treatment of endotoxemia. METHODS: (1) 96 BALB/c mice were divided into 2 groups: experimental group including 84 mice injected intraperitoneally with 17.5 mg/kg, LD(50) dose, of LPS mixed with lanthanum chloride of the dosages of 1 mg/kg, 2 mg/kg, 5 mg/kg, 10 mg/kg, 20 mg/kg, 40 mg/kg, and 80 mg/kg respectively; and control group including 12 mice injected intraperitoneally with 17.5 mg/kg of LPS. The mortality rates of different mice within 7 days were observed so as to observe the protective effect of lanthanum chloride. (2) 40 BALB/c mice were randomly divided into 2 group 2: experimental group injected intraperitoneally with lanthanum chloride of the dosages 10 mg/kg for 3 days and then injected with 1 LD(50) dosage of LPS 30 minutes after the last injection of lanthanum chloride of the dosages 10 mg/kg; and control group injected intraperitoneally with normal saline for 3 days and then with 1 LD(50) dosage of LPS 30 minutes after the last injection of normal saline. The mortality rates of different mice within 7 days were observed. (3) 40 BALB/c mice were randomly divided into 4 groups: LPS group, injected intraperitoneally with LPS of sublethal dosage (12.5 mg/kg), lanthanum chloride treatment group, injected intraperitoneally with LPS of sublethal dosage 1 hour after the venous injection of 10 mg/kg lanthanum chloride, lanthanum chloride control group, injected intravenously with 10 mg/kg lanthanum chloride, and NS control group, injected intraperitoneally with NS. Four hours after the intraperitoneal injection blood sample were collected to detect the plasma tumor necrosis factor-alpha (TNFalpha) and liver and thymus tissues were collected to examine the expression of TNFalpha mRNA and apoptosis of thymocytes by Rt-PCR and flow cytometry so as to observe the effects of lanthanum chloride on LPS-induced reaction in vivo. RESULTS: The mortality rates of the mice administrated with LD(50) dosage of LPS combined with 5, 10, and 20 mg/kg lanthanum chloride were 0, 0, and 8% respectively, all significantly lower than that of the control group (67%, all P < 0.01). The mortality rate of the LPS-challenged mice that were pretreated with 10 mg/kg of lanthanum chloride was 20%, significantly lower than that of the control group (55%, P < 0.05). (2) In the mice with endotoxemia that were pretreated with lanthanum chloride the plasma TNFalpha level was 0.44 +/- 0.22 ng/ml and the TNFalpha mRNA expression in liver was (3.93 +/- 0.62) x 10(5) copies/ micro g RNA, both significantly lower than those of the mice with endotoxemia without pretreatment of lanthanum chloride, 0.99 +/- 0.24 ng/ml and (1.9 +/- 0.33) x 10(7) copies/ micro g RNA (both P < 0.001). The percentage of DNA fragmentation of thymocytes in the mice challenged with LPS and pretreated with lanthanum chloride was 14.77% +/- 1.0%, significantly lower than that of the untreated mice (55.38% +/- 3.88%, P < 0.001), the percentage of hypodiploidy in thymocytes of the mice challenged with LPS was 15.56% +/- 0.59%, significantly higher than that of the lanthanum chloride treated mice (6.05% +/- 0.71%, P < 0.001). (3) Morphologic observation showed that pathological changes of the thymocytes and liver and lung tissues were remarkably milder in the lanthanum chloride-treated mice than in the mice challenged only by LPS. CONCLUSIONS: (1) Lanthanum chloride can bind LPS and reduce its toxicity, which shows protective effects on mice challenged by lethal dose LPS. (2) Lanthanum chloride can greatly decrease the secretion of TNFalpha and TNFalpha mRNA expression in the mice the secretion of TNFalpha and TNFalpha mRNA expression in the mice challenged with LPS. Furthermore, LPS-induced apoptosis of thymocyte and damage of liver and lungs are inhibited by lanthanum chloride.

Animals↗
PubMed1993

Toxicology and Carcinogenesis Studies of Mercuric Chloride (CAS No. 7487-94-7) in F344 Rats and B6C3F1 Mice (Gavage Studies).

Mercuric chloride is an inorganic compound that has been used in agriculture as a fungicide, in medicine as a topical antiseptic and disinfectant, and in chemistry as an intermediate in the production of other mercury compounds. The widespread use of mercury has resulted in increased levels of mercury in rivers and lakes. Mercuric chloride was evaluated in toxicity and carcinogenicity studies because of its extensive use and its occurrence as an environmental pollutant, and because of the lack of adequate long-term rodent studies. Toxicology and carcinogenesis studies were conducted by administering mercuric chloride (greater than 99% pure) in deionized water by gavage to groups of F344 rats or B6C3F1 mice for 16 days, 6 months, and 2 years. Genetic toxicology studies were conducted in Salmonella typhimurium (strains TA98, TA100, TA1535, and TA1537), in mouse lymphoma L5178Y cells, in Chinese hamster ovary cells, and in Drosophila melanogaster. 16-DAY STUDIES: Groups of five rats of each sex received 0, 1.25, 2.5, 5, 10, or 20 mg mercuric chloride/kg body weight and groups of five mice of each sex received 0, 5, 10, 20, 40, or 80 mg/kg in deionized water by gavage for 12 dose days. Two male rats in the 20 mg/kg group died in the first week, as did all male and four female mice from the 80 mg/kg group and one male mouse from the 40 mg/kg group. The final mean body weight of male rats receiving 20 mg/kg was 10% lower than that of the controls; the final mean body weight of 20 mg/kg females was 9% lower than that of the controls. Final mean body weights and body weight gains of dosed mice were similar to those of the controls. Absolute and relative kidney weights of male rats receiving 2.5 mg/kg or greater doses and of female rats administered 5 mg/kg or more were significantly greater than those of the controls. Absolute kidney weights of mice were significantly increased in all male dose groups and in the 40 mg/kg female dose group; relative kidney weights of dosed male and female mice were significantly greater than the controls. Analysis of kidney, liver, and brain tissues for mercury residues revealed that the highest mercury concentration was in the kidneys of rats and mice. Acute renal tubule nephropathy occurred in dosed rats and was slightly more severe in males than in females. Chemical-related lesions in mice included renal tubule necrosis, inflammation and necrosis of the forestomach, and necrosis of the glandular stomach. 6-MONTH STUDIES: Groups of 10 rats of each sex received 0, 0.312, 0.625, 1.25, 2.5, or 5 mg mercuric chloride/kg body weight in deionized water by gavage for 26 weeks. Groups of 10 mice of each sex received 0, 1.25, 2.5, 5, 10, or 20 mg/kg in deionized water by gavage for 26 weeks (males) or 27 weeks (females). No deaths related to mercuric chloride administration occurred in rats or mice. Mean body weight gains of male rats that received 5 mg/kg and all female rat dose groups that received 0.625 mg/kg or greater were significantly lower than the controls. The final mean body weight and body weight gain of male mice in the 20 mg/kg group were significantly lower than those of the controls; final mean body weights and body weight gains of other dosed male mice and all dosed female mice were similar to those of the controls. Absolute and relative kidney weights of all dosed male rats and of female rats that received 0.625 mg/kg or greater were significantly greater than those of the controls. In male mice, absolute kidney weights in the three highest dose groups were significantly increased; no biologically significant differences in organ weights occurred in female mice. Analysis of kidney, liver, and brain tissues for mercury residues revealed the highest mercury concentration in the kidneys of rats and mice. The severity of chronic nephropathy increased with dose in male rats. Cytoplasmic vacuolation of renal tubule epithelial cells was observed in male mice in the 5, 10, and 20 mg/kg groups. No histopathologic changes in female mice were related to chemical exposure. 2-YEAR STUDIES: Groups YEAR STUDIES: Groups of 60 rats of each sex received 0, 2.5, or 5 mg mercuric chloride/kg body weight and groups of 60 mice of each sex received 0, 5, or 10 mg/kg in deionized water by gavage 5 days per week for 2 years. The doses were based on decreased weight gains in rats receiving 10 and 20 mg/kg and the decreased weight in male mice receiving 40 mg/kg during the 16-day studies, and on the decreased weight gains and toxicity results seen in the 6-month studies. Increased absolute and relative kidney weights in rats and male mice in the 6-month studies and degenerative renal changes suggested that higher dose levels would result in inadequate survival rates for a 2-year study. 15-Month Interim Evaluations: Relative kidney weights were significantly increased in dosed rats and female mice. The severity of nephropathy was increased in male rats, but not in females. High-dose male and female rats had minimal to mild hyperplasia of the basal cell layer in the forestomach epithelium (diagnosed as acanthosis); this lesion was not found in control or low-dose rats. Male mice had an increased severity of vacuolation of the renal tubule epithelium; no chemical-related lesions occurred in the kidneys of females. The incidence of inflammation of the olfactory epithelium lining the nasal cavity increased in male and female high-dose mice. Survival, Body Weights, and Clinical Signs: Survival of dosed male rats was lower than that of the controls (26/50, 10/50, 5/50); survival of dosed female rats was similar to that of the controls (35/50, 28/49, 30/50). Although more than 60&percnt; of the mice in each dose group survived to study end, survival rates of high-dose male mice and dosed female mice were lower than those of the controls (males: 36/50, 36/50, 31/50; females: 41/50, 35/50, 31/50). The final mean body weights of high-dose male and female rats were 15&percnt; and 14&percnt; lower than controls, respectively. The mean body weight of low-dose female rats was generally similar to controls throughout the 2-year study; the mean body weight of low-dose male rats was similar to that of the control through week 89. In mice, mean body weights of all male and female dose groups were similar to those of the controls throughout the studies. Pathology Findings: Chronic nephropathy appeared to develop at an accelerated rate and led to decreased survival in both dosed male rat groups. Secondary effects of renal dysfunction in dosed male rats resulted in increased incidences of fibrous osteodystrophy of the bone, mineralization of various tissues, and parathyroid gland hyperplasia. Based on evaluations of single and step sections, the incidence of renal tubule hyperplasia was increased in high-dose male rats (control, 3/50; high-dose, 10/50), but the incidences of renal tubule adenoma in high-dose and control males were similar (4/50, 5/50). Renal tubule hyperplasia was also slightly increased in high-dose female rats (2/50, 5/50) and adenomas were seen in high-dose females, but not in controls (0/50, 2/50). Incidences of forestomach hyperplasia in rats were markedly increased in dosed males (3/49, 16/50, 35/50) and high-dose females (5/50, 5/49, 20/50). Squamous cell papillomas of the forestomach were found in 3 low-dose and 12 high-dose males and in 2 high-dose females. No squamous cell carcinomas were found. The incidence of thyroid follicular cell carcinoma was marginally increased in high-dose male rats (1/50, 2/50, 6/50). However, a corresponding increased incidence in follicular cell adenomas (1/50, 4/50, 0/50) or hyperplasia (2/50, 4/50, 2/50) in males did not occur, and the overall incidence of follicular cell neoplasms was not significantly increased (2/50, 6/50, 6/50). The incidence of nasal mucosa inflammation in male and female rats was increased in the high-dose groups (male: 9/50, 8/47, 18/50; female: 0/49, 5/49, 15/50) and may have been related to chemical administration. The incidences of mammary gland fibroadenomas were significantly decreased in dosed female rats (15/50, 5/48, 2/50). The incidence and severity of nephropathy were increased in dosed mice; secondary effects of renal dysfunction did not occur. Renal tubule hyperplasia was found in one control and two high-dose male mice. Two renal tubule adenomas and one renal tubule adenocarcinoma were seen in high-dose male mice. Additional step sections revealed focal hyperplasia in another control male; no additional renal tubule neoplasms were found in high-dose or control males. Proliferative lesions of the renal tubule epithelium were not found in female mice. The incidence of metaplasia of the olfactory epithelium increased with dose in male and female mice. No other biologically significant lesions were found. GENETIC TOXICOLOGY: Mercuric chloride was not mutagenic in Salmonella typhimurium strains TA100, TA1535, TA1537, or TA98 with or without exogenous metabolic activation (S9). Induction of sex-linked recessive lethal mutations in germ cells of male Drosophila melanogaster did not occur when mercuric chloride was administered in feed or by injection. However, positive results were obtained in mutagenicity tests with mammalian cells. In the absence of S9, mercuric chloride induced trifluorothymidine resistance in mouse L5178Y cells and chromosomal aberrations in Chinese hamster ovary cells. In the Chinese hamster ovary cell test for induction of sister chromatid exchanges, mercuric chloride produced a negative response without S9 and a weakly positive response in the presence of S9. CONCLUSIONS: Under the conditions of these 2-year gavage studies, there was some evidence of carcinogenic activity of mercuric chloride in male F344 rats based on the increased incidence of squamous cell papillomas of the forestomach. Marginally increased incidences of thyroid follicular cell adenomas and carcinomas may have been related to mercuric chloride exposure. There was equivocal evidence of carcinogenic activity of mercuric chloride in female F344 rats based on two squamous cell papillomas of the forestomach. There was equivocal evidence of carcinogenic activity of mercuric chloride in male B6C3F1 mice based on the occurrences of two renal tubule adenomas and one renal tubule adenocarcinoma. There was no evidence of carcinogenic activity of mercuric chloride in female B6C3F1 mice receiving 5 or 10 mg/kg. Nonneoplastic lesions associated with exposure to mercuric chloride included increased severity of nephropathy in male rats and male and female mice. There was an increased incidence of renal tubule hyperplasia in male rats. The incidence of forestomach hyperplasia was increased in dosed male and female rats. Increased incidences of nasal mucosa inflammation were associated with mercuric chloride administration in rats. Increased incidences of olfactory epithelial metaplasia in mice were also associated with mercuric chloride administration. Synonyms: Abavit B, calochlor, corrosive sublimate, dichloromercury, mercuric bichloride, mercury chloride, mercury (II) chloride, mercury bichloride, mercury perchloride, sublimate, sulem, bichloride of mercury, corrosive mercury chloride, perchloride of mercury, mercury dichloride Trade name: Fungchex

Journal Article↗