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Biomedical subjects

H Fritz

Publications and source records attributed to H Fritz.

At least 361 records · Page 20Linked to original sources

Toxicity of chlorobenzene on Pseudomonas sp. strain RHO1, a chlorobenzene-degrading strain.

Pseudomonas sp. strain RHO1 able to use chloro- and 1,4-dichlorobenzene as growth substrates was tested towards sensitivity against chlorobenzene. Concentrations of chlorobenzene higher than 3.5 mM were found to be toxic to cells independent of pregrowth with chlorobenzene or nutrient broth. Below this concentration, sensitivity towards chlorobenzene depended on the precultivation of the cells, i.e. type of growth substrate (chlorobenzene or nutrient broth) and the concentration of chlorobenzene as the growth substrate. Cells grown in continuous culture were especially sensitive with a threshold concentration of 2.5 mM chlorobenzene. In addition to chlorobenzene, metabolites also seem to function as toxic compounds. 2-Chlorophenol and 3-chlorocatechol were isolated from cell extracts. Cleavage of 3-chlorocatechol by catechol 1,2-dioxygenase seems to be the critical step in the metabolism of chlorobenzene.

Biodegradation, Environmental↗

Comparative study of the teratogenicity of phenobarbitone, diphenylhydantoin and carbamazepine in mice.

Three selected anticonvulsants, phenobarbitone (PHB), diphenylhydantoin (DPH) and carbamazepine (CAA) were examined for embryotoxic and teratogenic activity in albino mice. After oral treatment of the dams during the period of organogenesis (days 6-15 of gestation) with both PHB and DPH in doses causing marked symptoms and signs of toxicity (40 and 170 mg/kg/day respectively), an abnormally high incidence of cleft palate was observed in the foetuses (4.3% and 9.3% resp.). In a cumulative control group of foetuses, the incidence of this particular malformation was only 0.13%. No significant change in the malformation rate was seen after the administration of CAA in doses up to 250 mg/kg/day. Slight to moderate retardation of foetal growth was noted after treatment with DPH and CAA, but only at the higer and toxic dose levels. DPH also increased the incidence of early embryonic deaths (deciduomata).

Abnormalities, Drug-Induced↗

Release of granulocyte proteinases during hemodialysis.

Neutral proteinases of neutrophilic polymorphonuclear leukocytes were followed up cytochemically in blood smears of 12 patients submitted to regular hemodialysis treatment (RDT). Halo formation (ring-shaped area around each neutrophil due to protein degradation) was reduced in all patients with end-stage renal disease under RDT. Concomitant to the development of leukopenia, a maximal increase of the plasma levels of the granulocytic elastase in complex with alpha 1-proteinase inhibitor was observed 3 h after starting hemodialysis (+409%; p less than 0.001). On the other hand, the proteolytic activity of the plasma samples against azocasein as substrate, being significantly higher (+244%; p less than 0.001) in RDT patients compared with healthy controls, decreased permanently during therapy (-71%; p less than 0.001; 3 h after initiation of the treatment). The mechanisms of release as well as of elimination of proteolytic activity due to RDT are discussed.

Adult↗