Search PubMed⌕ Search

Biomedical subjects

G C Becking

Publications and source records attributed to G C Becking.

At least 37 records · Page 2Linked to original sources
PubMed1980

Short-term study of the combined effects of mirex, photomirex, and kepone with halogenated biphenyls in rats.

The combined effects of polychlorinated biphenyls (PCBs) or a polybrominated biphenyl (PBB) with mirex, kepone, or photomirex were investigated in rats. Groups of 10 animals were fed diets containing the organohalogens alone or in various combinations for 28 d. Body weight gain and food consumption were not affected by any treatment. Liver weight was increased in the group fed Aroclor 1260/photomirex and in all groups receiving PBB. Hepatic microsomal enzyme activities were elevated in the groups treated with halogenated biphenyls alone; this effect was not potentiated in the presence of mirex-related compounds. Serum biochemical parameters were, for the most part, normal. Hematology tests revealed no abnormalities. Histological changes occurred in the liver, thyroid, and kidney of rats treated with the organohalogens alone or in combination. Liver alterations consisted of central lobular cytoplasmic enlargement, exaggerated periportal perinuclear halos, and increased nuclear hyperchromicity and anisokaryosis. Fatty degeneration was observed in all treated groups. Thyroid changes were characterized by a generalized reduction in follicular size and colloid density with collapse of the follicles. Kidneys suffered mild eosinophilic cytoplasmic inclusions in the proximal convoluted tubule and focal lymphoid aggregates. Histological changes due to PCBs and PBB were aggravated by mirex and related compounds. The degree of damage appeared to be additive rather than potentiative. Mirex and photomirex levels in livers of rats concomitantly exposed to halogenated biphenyls were four to six times higher than those in rats fed mirex-related compounds alone. However, the toxic response in this organ was not potentiated as a result of the increased accumulation. It was concluded that mirex-related compounds at the dose levels studied did not potentiate the effects produced by halogenated biphenyls and vice versa.

Animals↗
PubMed1980

Tissue distribution and elimination of 2,8-dihydromirex in the rat.

The tissue distribution and elimination kinetics of 14C-labeled dihydromirex were investigated in the rat. Dihydromirex was distributed in all tissues examined after iv or oral administration; the highest concentrations were found in the fat, liver, and skin. The pattern of distribution was similar to that of photomirex and mirex. Elimination of dihydromirex from the blood after an iv dose was expressed by a four-compartment model, whereas fecal excretion was represented by a biphasic curve. Excretion of dihydromirex occurred predominantly in the feces; only minute amounts were found in the urine and bile. Dihydromirex constituted 90-100% of the total radioactivity in tissues and feces. No metabolite was detected.

Adipose Tissue↗
PubMed1980

Subchronic toxicity of photomirex in the female rat: results of 28- and 90-day feeding studies.

Photomirex (8-monohydromirex) was administered to female Sprague-Dawley rats at dietary levels of 0.2, 1.0, 5.0, 25.0 and 125 ppm. Food intake and body weight gain were significantly depressed at the 125 ppm level in the 28- but not in the 90-day study. Significant alterations were observed in some hematological and biochemical parameters at the highest dietary level in the 90-day study. Photomirex residues accumulated in a dose-dependent manner in perirenal fat, liver, brain, kidney, and spleen. Dose-dependent histotoxic effects were observed in liver and thyroid at and above 1 ppm; hepatomegaly was observed at 25.0 and 125 ppm. These results indicate that photomirex was approximately five times more toxic than mirex in terms of liver histology. When these results are compared with those observed in an earlier study in the male rat, it is evident that the female is less susceptible to photomirex than the male.

Adipose Tissue↗
PubMed1976

Hepatic drug metabolism in iron-, magnesium- and potassium-deficient rats.

It is now apparent that the rate of microsomal drug metabolism in experimental animals is subject to alteration by such dietary deficiencies as protein, vatamins, fats and minerals. The evidence, both published and unpublished, showing the effects of iron, magnesium, and potassium dificiencies on the hepatic metabolism of foreign compounds in rats is discussed. Iron deficiency has been shown to lead to a marked stimulation in hepatic metabolism, in vitro and in vivo, of both Type I (aminopyrine) and Type II (aniline) substrates. Magnesium-deficient rats have been shown to have markedly lower in vivo and in vitro rates of hepatic drug metabolism, but the monovalent intracellular mineral potassium had no apparent effect on the in vitro enzymatic conversion of foreign compounds. Hypokalemia has been shown to alter the in vivo disposition of aminopyrine and pentobarbital as evidenced by an increased plasma half-life of aminopyrine and a longer pentobarbital sleeping time in potassium-deficient animals. Large segments of the world's population are in less than satisfactory nutritional status with respect to iron, magnesium, potassium, copper, and zinc and the relevancy to man of the data discussed must be ascertained. The role of dietary minerals in nonhepatic microsomal drug metabolism is also not yet known.

Aminopyrine N-Demethylase↗