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Int Arch Occup Environ Health. 2000 Nov;73(8):528-36.
Isopropanol and methylformate exposure in a foundry: exposure data and neurobehavioural measurements.

Sethre T, Laubli T, Hangartner M, Berode M, Krueger H.

Institute of Hygiene and Applied Physiology, Zurich, Switzerland. sethrha.bepr.ethz.ch

OBJECTIVES: The aim of this study was to determine the dose-effect relationship between solvent exposure and acute neurobehavioural effects at the worksite. METHODS: In a balanced design, ten workers in a Swiss foundry were monitored for 15 days at ten different times during work. Urine samples were taken in the morning and at the time of examination, and personal exposure to isopropanol and methylformate was measured with active samplers. Neurobehavioural tests such as postural balance (bipedal, bipedal blind, monopedal), simple reaction time and digit span of the Neurobehavioural Evaluation System (NES2) and a combined memory and reaction-time test, the combi-test, were performed. A rating of well-being, and the last consumption of alcohol, caffeine, nicotine and medication were reported. RESULTS: Average environmental concentrations of isopropanol were at 44 ppm ( +/- 16 ppm), and at 36 ppm (+/-21 ppm) for methylformate. Maximum values of personal exposure to isopropanol reached barely the maximal allowable concentration (MAC) value (400 ppm); the methylformate personal exposure of three workers exceeded the MAC value (100 ppm). Urine concentrations of methanol were high (3.1 +/- 2.3 mg/l in the morning, 7.8 +/- 4.9 mg/l after exposure) compared with the results of other studies; concentrations of isopropanol were rather low (0.88 +/- 0.73 mg/l after exposure). CONCLUSIONS: Nevertheless, between personal exposure and biomonitoring, linear correlation was found. Methylformate exposure correlated with methanol and formic acid concentration in the urine, and isopropanol exposure with its concentration in the urine. With the neurobehavioural tests used, no solvent effect in relation to the dose could be determined.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11100947&dopt=Abstract

J Physiol. 2000 Dec 1;529 Pt 2:307-19.
Functional IP3- and ryanodine-sensitive calcium stores in presynaptic varicosities of NG108-15 (rodent neuroblastoma x glioma hybrid) cells.

Ronde P, Dougherty JJ, Nichols RA.

Departments of Pharmacology and Physiology, and Neurobiology and Anatomy, Medical College of Pennsylvania Hahnemann University, Philadelphia, PA 19102, USA.

Presynaptic varicosities of the model neuronal cell line NG108-15, a cholinergic neuroblastoma cell x glioma cell hybrid capable of innervating striated myotubes, were examined for the presence of inositol 1,4,5-trisphosphate (IP3)-sensitive and Ca2+-activated (ryanodine-sensitive) Ca2+ stores using confocal microscopic imaging of Ca2+-sensitive fluorescent dye loaded into the cells. Initial demonstration of the presence of IP3 receptors and ryanodine receptors in the NG108-15 varicosities was obtained using immunocytochemistry. Treatment of NG108-15 cells with bradykinin (0.1 microM), whose receptor is linked to IP3 generation, and separately, caffeine (10 mM), an activator of endoplasmic reticulum ryanodine receptors, resulted in substantial increases in [Ca2+]i in the varicosities. K+-evoked changes in [Ca2+]i in the varicosities were reduced (52 %) after emptying the ryanodine-sensitive Ca2+ store using caffeine (10 mM), but were not affected by prior depletion of the IP3-sensitive Ca2+ store using thapsigargin (1 microM). Bradykinin-induced changes in [Ca2+]i were abolished following depletion of the IP3-sensitive Ca2+ store using thapsigargin (1 microM) and were reduced (72 %) by prior emptying of the ryanodine-sensitive Ca2+ store with caffeine (10 mM). The same results were obtained when the varicosities of the NG108-15 cells had formed synaptic junctions with co-cultured rat hindlimb myotubes. Taken together, the results suggest that, in the varicosities, activation of the IP3 pathway evoked the release of Ca2+ from the IP3-sensitive store, which, in turn, secondarily induced the release of Ca2+ from the ryanodine-sensitive store via Ca2+-induced Ca2+ release, and that depolarization-induced Ca2+ entry evoked Ca2+-induced Ca2+ release only from the ryanodine-sensitive store. Thus, functional internal Ca2+ stores are inherent components of presynaptic varicosities in this neural cell line.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11101642&dopt=Abstract

J Physiol. 2000 Dec 1;529 Pt 2:395-404.
Regulation of basal intracellular calcium concentration by the sarcoplasmic reticulum in myocytes from the rat gastric antrum.

White C, McGeown JG.

Smooth Muscle Research Group, Department of Physiology, Queen's University of Belfast, 97 Lisburn Road, Belfast BT9 7BL, UK.

The intracellular calcium concentration ([Ca2+]i) was monitored in fura-2-loaded myocytes isolated from the rat gastric antrum and voltage clamped at -60 1r1rqmV1qusing the perforated patch clamp technique. The rate of quench of fura-2 fluorescence by Mn2+ was used as a measure of capacitative Ca2+ entry. Cyclopiazonic acid (5 microM) did not affect the holding current but produced a sustained elevation in steady-state [Ca2+]i that was dependent on the presence of external calcium. Cyclopiazonic acid increased Mn2+ influx with physiological external [Ca2+], but not in Ca2+-free conditions. Cyclopiazonic acid increased the rate of [Ca2+]i rise following a rapid switch from Ca2+-free to physiological [Ca2+] solution. Sustained application of carbachol (10 microM) produced an elevation in steady-state [Ca2+]i that was associated with an increased rate of Mn2+ influx. Application of cyclopiazonic acid in the presence of carbachol further elevated steady-state [Ca2+]i without changing Mn2+ influx. Ryanodine (10 microM) elevated steady-state [Ca2+]i either on its own or following a brief application of caffeine (10 9i1s1sqmMc1q). Cyclopiazonic acid had no further effect when added to cells pre-treated with ryanodine. Neither caffeine nor ryanodine increased the rate of Mn2+ influx. When brief applications of ionomycin (25 microM) in Ca2+-free solution were used to release stored Ca2+, ryanodine reduced the amplitude of the resulting [Ca2+]i transients by approximately 30 %, indicating that intracellular stores were partially depleted. These findings suggest that continual uptake of Ca2+ by the sarcoplasmic reticulum Ca2+-ATPase into a ryanodine-sensitive store limits the bulk cytoplasmic [Ca2+]i under resting conditions. This pathway can be short circuited by 10 microM ryanodine, presumably by opening Ca2+ channels in the sarcoplasmic reticulum. Depletion of stores with cyclopiazonic acid or carbachol also activates capacitative Ca2+ entry.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11101649&dopt=Abstract

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