Biomedical subjects

J de Ceaurriz

Publications and source records attributed to J de Ceaurriz.

39 records · Page 3Linked to original sources

PubMedDate not supplied

Triethylbenzene-induced sensorimotor neuropathy in rats.

1,2,4-Triethylbenzene (1,2,4-TEB) and 1,3,5-triethylbenzene (1,3,5-TEB) were administered orally to male Sprague-Dawley rats. Experimental and appropriate control rats were examined electrophysiologically for motor and sensory conduction velocities (MCV and SCV), and the amplitudes of the sensory (ASAP) and muscular action potentials (AMAP), at bi-weekly intervals. Oral administration of 1,2,4-TEB (200 or 400 mg kg-1, once daily, 4 days per week for 8 weeks) produced a time- and dose-dependent decrease in MCV, SCV, AMAP and ASAP. Rats treated with 1,2,4-TEB exhibited a bluish discoloration of the skin and the urine was greyish-greenish. No changes in MCV, SCV, AMAP and ASAP developed in rats given 1,3,5-TEB orally (200 or 400 mg kg-1, daily, 4 days per week for 8 weeks). The results indicate that 1,2,4-TEB is a neurotoxic isomer of TEB and that the presence of two ethyl radicals in the ortho-position on an aromatic ring could be a critical molecular arrangement resulting in chromogenic and neurotoxic properties.

Action Potentials↗

PubMedDate not supplied

Urinary thiodiglycolic acid and thioether excretion in male rats dosed with 1,2-dichloroethane.

1,2-dichloroethane (DCE) is extensively metabolized and partially excreted in urine as thioether compounds, which include thiodiglycolic acid (TDGA). In this study, we have compared the urinary excretion of TDGA and thioethers in the rat after administration of increasing doses of DCE. Male Sprague Dawley rats were given a single oral dose of labelled [14C]DCE (0.125 to 8.08 mmol kg-1 body wt.) and 24-h urine samples were collected. The TDGA and thioethers were determined in urine by a gas chromatography method and by the thioether assay after alkaline hydrolysis, respectively. The percentage of the administered radioactivity that was excreted in urine decreased with increasing dose of DCE and ranged between 63 and 7.4%. The amount of TDGA increased proportionally to the DCE dose up to 1.01 mmol DCE kg-1 body wt. and corresponded to 0.22 mmol TDGA mmol-1 DCE. Up to 0.25 mmol DCE kg-1 body wt., the amount of thioethers recovered in urine was not significantly different as compared to the vehicle control group (11.8 +/- 0.6 mumol SH equiv. kg-1 body wt., n = 10). From the 0.25-4.04 mmol DCE kg-1 body wt. dose, the amount of thioethers increased linearly with the dose of DCE and corresponded to 0.028 mmol SH equiv. mmol-1 DCE. The ratio between urinary thioethers and TDGA increased with the DCE dose and reached 0.17 +/- 0.01 (n = 5) at a dose of 8.08 mmol DCE kg-1 body wt. Moreover, TDGA contents determined in urine by gas chromatography before and after alkaline hydrolysis were not significantly different.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMedDate not supplied

Role of extracellular glutathione and gamma-glutamyltranspeptidase in the disposition and kidney toxicity of inorganic mercury in rats.

The role of extracellular glutathione (GSH) and membrane-bound gamma-glutamyltranspeptidase (gamma-GT) as contributory factors in the disposition and toxicity of inorganic mercury (HgCl2, 1 mg kg-1, i.p.) was investigated in rats pretreated with acivicin (AT-125, 10 mg kg-1), a gamma-GT inhibitor. A high degree of gamma-GT inhibition (75%) and of protection (90%) against HgCl2-induced nephrotoxicity was obtained in gamma-GT-inhibited rats 24 h post-treatment. Pretreatment with acivicin affected the fractional distribution profile of 203 Hg, resulting in a twofold decrease in the renal incorporation of mercury 4 h post-treatment and a threefold increase in the 24-h urinary excretion of mercury. Plasma radioactivity remained constant over 24 h in rats dosed with 203Hg alone, whereas it decreased by 60% between 4 h and 24 h in gamma-GT-inhibited rats. In gamma-GT-inhibited rats treated with HgCl2 the renal and plasma reduced glutathione (GSH) content increased by 68% and 330% respectively, as compared to controls. The gamma-GT inhibition affected the distribution profile of mercury within urinary proteins, shifting the binding of mercury from the high-molecular-weight fraction (3% against 80%) to the low-molecular-weight fraction (72% against 10%). A significant but less impressive shift of mercury from the high- to the low-molecular-weight fraction also arose in the plasma. These results taken together support the pivotal role of extracellular GSH and membrane-bound gamma-GT in the renal incorporation, toxicity and excretion of inorganic mercury in rats.

Animals↗