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Biomedical subjects

M Rodamilans

Publications and source records attributed to M Rodamilans.

36 records · Page 2Linked to original sources
PubMed1992

Sulphur derivative of hexachlorobenzene in human urine.

Pentachlorothiophenol, a sulphur derivative of the widespread environmental pollutant hexachlorobenzene (HCB) has been detected and quantified in the urine of a human general population with high body burden of HCB. The sulphur derivative was analysed by GLC-MS as pentachlorothioanisole (PCTA) after hydrolysis and methylation of the respective conjugate and was found in 100% of the samples (n = 40) with a mean concentration of 1.85 +/- 0.98 ng ml-1 (mean +/- s.d., range 0.58-4.50 ng ml-1). No correlation with urinary pentachlorophenol (PCP) and no sex-related differences were found. The derivative may originate from the biotransformation of HCB stored in tissues and may be a useful maker of HCB metabolism in humans.

Biotransformation↗
PubMed1991

Transport of organochlorine residues in the rat and human blood.

Organochlorine residues (OCR)2 are poorly soluble in water and are transported in the organism bound by the blood components. The distribution among blood fractions (cells/plasma, lipoproteins/rest of plasma proteins) were variable depending on the residue (HCB, p p'-DDE, HCH, Aroclor 1260, PCP) and on the species (rat, man). Differences were not found between in vivo (after oral single dosing) and in vitro (blood incubation) experiments. Results indicated a high affinity of organochlorine residues for lipoproteins; however, binding to blood carriers was very weak as demonstrated by the rapid release of residues by elution through a reverse phase column. The effects of residue binding to blood components on the distribution kinetics to tissues are discussed.

Administration, Oral↗
PubMed1991

Studies on sex differences in excretion of sulphur derivatives of hexachlorobenzene and pentachloronitrobenzene by rats.

The appearance of sex-related differences in the excretion of sulphur derivatives of hexachlorobenzene (HCB) and pentachloronitrobenzene (PCNB) was studied in vitro and in vivo. Sexually immature rats given HCB showed initially no differences in the excretion of N-acetyl-S-(pentachlorophenyl)cysteine, but 5-8 days after weaning the urinary levels of the sulphur derivative began to increase in females until a 10-fold difference between both sexes was established. The studies in vitro and the analysis of tissues after in vivo administration of PCNB showed that conjugation with glutathione and hydrolysis of the conjugates to yield free pentachlorothiophenol do not present sex-related differences. These data tend to reinforce the view that an active renal secretory mechanism probably induced by estrogens during sexual maturation is responsible for the highly efficient excretion of sulphur derivatives of HCB and PCNB by female rats.

Administration, Oral↗
PubMed1989

[Failure of a cyclophosphamide-dexamethasone combination in paraquat poisoning].

A 37-year-old female deliberately ingested a 20% solution of paraquat in water. One hour later gastric lavage was carried out and bentonite was administered. Five hours later cyclophosphamide (5 mg/kg/day) and dexamethasone (24 mg/day) were started and a continuous intestinal lavage was carried out; four hours later, hemodialysis was begun. After 36 hours, features of renal and respiratory failure developed, with a rapid progress to respiratory distress. The patient died 94 hours after the ingestion of the poison. Despite early therapy with dexamethasone and cyclophosphamide, this patient's evolution does not support the presumed effectiveness of this drug association for paraquat poisoning.

Adult↗
PubMed1989

Effects of cimetidine on gastric alcohol dehydrogenase activity and blood ethanol levels.

Chronic use of cimetidine and alcohol are commonly associated, but studies on their interactions are the subject of controversy. To investigate this question, a small ethanol dose (0.15 g/kg body wt) was randomly administered on 2 consecutive days either orally or intravenously to 6 normal volunteers, before and after 1 wk of oral administration of 400 mg of cimetidine twice daily. Although cimetidine did not change the areas under the curve of blood ethanol concentrations after intravenous administration, those after oral alcohol intake were twice as large with cimetidine than without. Similar effects were reproduced in rats after intravenous administration of cimetidine (50 mg/kg body wt). In vitro, cimetidine was a noncompetitive inhibitor of gastric alcohol dehydrogenase activity at concentrations as low as 0.01 mM, 100-fold lower than those needed to inhibit the hepatic dehydrogenase. These results indicate that gastric alcohol dehydrogenase activity governs, in part, the systemic bioavailability of ethanol. Consequently, systemic effects of alcohol may be exacerbated in patients receiving cimetidine.

Adult↗
PubMed1988

Mobilization of stored hexachlorobenzene and p,p-dichlorodiphenyldichloroethylene during partial starvation in rats.

Hexachlorobenzene (HCB) and p,p'-dichlorodiphenyldichloroethylene (p,p'-DDE) kinetics were compared in rats before, during and after partial starvation. Food restriction produced a drastic mobilization of the residues stored in the adipose tissue resulting in symptoms of neurotoxicity. The redistribution was reversible and did not produce a significant reduction in the chemicals body burden. HCB and p,p'-DDE, although both highly lipophilic, showed important differences in their blood transport and distribution pattern, with more HCB being transported by red blood cells and with a greater facility for HCB to reach the liver and the brain.

Adipose Tissue↗
PubMed1988

Inhibition of intratesticular testosterone synthesis by inorganic lead.

The alterations in testicular testosterone synthesis produced by exposure to inorganic lead were investigated in BALB/c+ mice. Lead concentration in blood and testes and the levels of testosterone and delta 4-androgen biosynthesis pathway precursors (4-androstenedione, 17-hydroxyprogesterone, and progesterone) were measured in animals which were exposed to lead acetate in the drinking water (366 mg/l, 0.97 +/- 0.12 mg lead/animal/day) during 6 months. The results showed a significant reduction of the intratesticular testosterone levels after 30 days of exposure and of the androstenedione levels after 150 days. Intratesticular progesterone and hydroxyprogesterone levels showed no changes during the assay.

Androgens↗
PubMed1988

Lead toxicity on endocrine testicular function in an occupationally exposed population.

The hypothalamo-pituitary-testicular axis was evaluated in a group of 23 men who worked in the lead smelting industry and had a history of occupational inorganic lead exposure. The endocrine status of the workers was related to lead poisoning biological markers. According to the duration of their lead exposure they were divided into three groups: group 1 less than 1 year, n = 5; group 2 between 3 and 5 years, n = 8; group 3 greater than 5 years, n = 10. Serum testosterone (T), steroid binding globulin (SBG), free testosterone index (T/SBG), serum luteinizing hormone (LH), follicle stimulating hormone (FSH), Blood lead levels, and blood zinc protoporphyrin (ZPP) were measured in all workers. Groups 2 and 3 showed a decrease in serum testosterone levels, an increase in SBG levels, and a decrease in T/SBG index, suggesting a correlation between testicular dysfunction and duration of exposure. There was an increase in serum LH in group 1, which was not progressive. This suggests that prolonged lead exposure initially produces a direct testicular toxicity followed by hypothalamic or pituitary disturbance when longer periods of exposure take place.

Adult↗
PubMed1987

Pentachlorophenol and hexachlorobenzene in serum and urine of the population of Barcelona.

1 Urinary chlorophenols of the general population of Barcelona, Spain were determined. Pentachlorophenol (PCP: 25.0 +/- 3.9 ng/ml; mean +/- s.e.m., n = 50) and tetrachlorophenol (TCP: 6.2 +/- 1.6 ng/ml; mean +/- s.e.m., n = 25) were found in all samples. 2 Pentachlorophenol and hexachlorobenzene were also determined in serum. Both were present in all samples (PCP: 21.9 +/- 1.9 ng/ml; HCB: 11.1 +/- 1.1 ng/ml; mean +/- s.e.m., n = 100). Their concentrations do not show any correlation, suggesting no metabolic relation between them.

Chlorobenzenes↗
PubMed1986

Sulindac reduces the urinary excretion of prostaglandins and impairs renal function in cirrhosis with ascites.

In 5 patients with cirrhosis and ascites the glomerular filtration rate (GFR), free water clearance (CH2O) and urinary excretion of prostaglandin E2(PGE2) and 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha) were measured before and after a 3-day treatment with sulindac (400 mg/day). The administration of sulindac induced a marked fall of urinary excretion of PGE2 (from 24.2 +/- 5.5 to 3.8 +/- 1.1 ng/h; p less than 0.05), 6-keto-PGF1 alpha (from 19.9 +/- 2.9 to 5.6 +/- 1.1 ng/h; p less than 0.02) GFR (from 111 +/- 15 to 67 +/- 10 ml/min; p less than 0.01) and CH2O (from 7 +/- 1.5 to 3.7 +/- 1.3 ml/min; p less than 0.02) in all patients studied. The plasma concentration of the active metabolite sulindac sulfide in cirrhotics was 400% of that found in 6 healthy volunteers (9.6 +/- 1.7 vs. 2.4 +/- 0.6 ng/ml). Our results indicate that sulindac, at a dose of 400 mg/day, inhibits the renal synthesis of prostaglandins and impairs renal function in cirrhotics with ascites. These effects are probably related to the marked alteration of sulindac kinetics that occurs in these patients.

6-Ketoprostaglandin F1 alpha↗
PubMed1986

Mobilization, redistribution and excretion of hexachlorobenzene following food restriction in rats.

Adult female rats were given a single oral dose of hexachlorobenzene (HCB) (100 mg/kg, 1% carboxy methyl cellulose) by stomach tube. Six days after HCB dosage the diet of the animals was restricted to 30% of their normal intakes for 7 days. Following dosage and during partial starvation faecal elimination of HCB was monitored. The animals were killed on day 13 and their tissues removed for HCB analysis. A significant increase in HCB was found in all tissues, notably in the brain (367%) and the liver (496%), with HCB being mobilized from fat depots to plasma and then redistributed. The pattern of HCB faecal elimination suggests that food restriction enhances non-biliary excretion, correlating with plasma levels and faecal volume.

Animals↗
PubMed1984

Effect of demeclocycline on renal function and urinary prostaglandin E2 and kallikrein in hyponatremic cirrhotics.

8 cirrhotics with hyponatremia were given demeclocycline (DMC) 900 mg/day to investigate its effect on renal function, plasma renin activity, aldosterone and urinary excretion of prostaglandin E2 and kallikrein. In 7 patients DMC induced an increase of free water clearance (from -0.36 +/- 0.06 to 0.13 +/- 0.06 ml/min) and serum sodium concentration (from 125.4 +/- 0.09 to 131.1 +/- 1.0 mEq/l, mmol/l). In 5 of these patients DMC also induced a marked reduction of glomerular filtration rate (from 72.2 +/- 6.2 to 31,2 +/- 4.7 ml/min) and renal plasma flow (from 468 +/- 98 to 195 +/- 55 ml/min) which could not be explained on the basis of hypovolemia. In each case this renal impairment was not associated with changes in urinary concentration of beta 2-microglobulin, urinary casts excretion, fresh urine sediment or urine protein content and disappeared after discontinuation of the drug. DMC induced a marked increase in the urinary excretion of prostaglandin E2 (from 0.82 +/- 0.27 to 6.16 +/- 1.91 ng/min) in 6 out of the 7 patients who responded to DMC and a marked reduction in urinary kallikrein (from 16.1 +/- 4.4 to 4.2 +/- 1.6 pkat/min) in the 5 patients who developed renal insufficiency. The serum DMC concentration was greater than 5 micrograms/ml in all patients who responded to DMC, greater than 8 micrograms/ml in all cases who developed renal insufficiency and of 3 micrograms/ml in the case not responding to DMC. (ABSTRACT TRUNCATED AT 250 WORDS)

Acute Kidney Injury↗
PubMedDate not supplied

Serum selenium concentration of a healthy northwest Spanish population.

Selenium (Se) is an essential element, cofactor for glutathione peroxidase (GSHPx) activity, whose deficiency may induce modifications in the cellular antioxidative status and induce the appearance of different diseases. Current views suggest that a serum Se concentration inferior to 45 micrograms/L may correlate with an increased risk of coronary hearth diseases, coronary atherosclerosis and cancer. Since the Se concentration in human blood varies between geographical areas, we initiated a study to evaluate the Se status in the general healthy population of Barcelona. Serum Se concentration was investigated in a random sample of 150 subjects (age range 18-70 yr) by graphite furnace atomic spectrometry (FLAAS). L'vov platform, Zeeman background correction, and other specifications of stabilized temperature platform furnace (STPF) concept were followed. The results show that in the general population of Barcelona, Se serum concentration ranges between 60 and 106 micrograms/L (X = 80.7 +/- 10 micrograms/L). These values can be considered within the safe limits, since no subject was found with a concentration lower than the threshold of 45 micrograms/L.

Adolescent↗