Benoxaprofen suppression of polychlorinated biphenyl toxicity without alteration of mixed function oxidase function

Nature ◽  
1983 ◽  
Vol 303 (5917) ◽  
pp. 524-526 ◽  
Author(s):  
Arleen B. Rifkind ◽  
Haidrun Muschick
Keyword(s):  
Polychlorinated Biphenyl ◽  
Mixed Function Oxidase

Fine Structural Alterations in Thyroid Follicular Cells (FC) and Changes in Serum Thyroxine Produced by Feeding Polychlorinated Biphenyl (PCB) to Rats

1977 ◽  
Vol 35 ◽  
pp. 498-499
Author(s):  
W.T. Collins ◽  
Charles C. Capen ◽  
Louis Kasza
Keyword(s):  
Feed Efficiency ◽  
Polychlorinated Biphenyl ◽  
Serum Proteins ◽  
Skin Lesions ◽  
Hepatic Necrosis ◽  
Ultrastructural Changes ◽  
Lymphoid Tissues ◽  
Heat Transfer Fluids ◽  
Thyroid Follicular Cells ◽  
Peripheral Metabolism

The widespread contamination of the environment with PCB, a compound used extensively by industry in hydraulic and heat transfer fluids as well as plasticizers and solvents in adhesives and sealants, has resulted in detectable tissue levels in a large portion of the human population, domestic animals, and wildlife. Intoxication with PCB produces severe hepatic necrosis, degeneration of lymphoid tissues and kidney, skin lesions, decreased reproductive performance, reduced feed efficiency, and decreased weight gain. PCB also has been reported to reduce the binding of thyroid hormone to serum proteins and enhance the peripheral metabolism of thyroxine with increased excretion of thyroxine-glucuronide in the bile (Bastomsky, Endocrinology 95: 1150-1155, 1974).The objectives of this investigation were (1) to investigate the histopathologic, histochemical, and ultrastructural changes in thyroid FC produced by the acute (4 week) and chronic (12 week) administration of low (50 ppm) and high (500 ppm) doses of PCB to rats, (2) to correlate these alterations to changes in serum immunoreactive thyroxine concentration, and (3) to investigate the persistence of the effects of PCB on the thyroid gland.

Ultrastructure and Drug Metabolism in the Developing Guinea Pig

1973 ◽  
Vol 31 ◽  
pp. 538-539
Author(s):  
W. Kuenzig ◽  
M. Boublik ◽  
J.J. Kamm ◽  
J.J. Burns
Keyword(s):  
Guinea Pig ◽  
Metabolic Activity ◽  
Animal Species ◽  
Adult Animal ◽  
Smooth Endoplasmic Reticulum ◽  
Fetal Life ◽  
Mixed Function Oxidase ◽  
Cytochrome P 450 ◽  
Microsomal Mixed Function Oxidase ◽  
Mixed Function Oxidase Activity

Unlike a variety of other animal species, such as the rabbit, mouse or rat, the guinea pig has a relatively long gestation period and is a more fully developed animal at birth. Kuenzig et al. reported that drug metabolic activity which increases very slowly during fetal life, increases rapidly after birth. Hepatocytes of a 3-day old neonate metabolize drugs and reduce cytochrome P-450 at a rate comparable to that observed in the adult animal. Moreover the administration of drugs like phenobarbital to pregnant guinea pigs increases the microsomal mixed function oxidase activity already in the fetus.Drug metabolic activity is, generally, localized within the smooth endoplasmic reticulum (SER) of the hepatocyte.

Polychlorinated biphenyl induced hepatocyte alterations

1987 ◽  
Vol 45 ◽  
pp. 716-717
Author(s):  
D.N. Collins ◽  
J.N. Turner ◽  
K.O. Brosch ◽  
R.F. Seegal
Keyword(s):  
Lipid Droplets ◽  
Wistar Rats ◽  
Homovanillic Acid ◽  
Polychlorinated Biphenyl ◽  
Corn Oil ◽  
Environmental Pollutants ◽  
Short Term ◽  
Pcb Congeners ◽  
Urinary Levels ◽  
The Brain

Polychlorinated biphenyls (PCBs) are a ubiquitous class of environmental pollutants with toxic and hepatocellular effects, including accumulation of fat, proliferated smooth endoplasmic recticulum (SER), and concentric membrane arrays (CMAs) (1-3). The CMAs appear to be a membrane storage and degeneration organelle composed of a large number of concentric membrane layers usually surrounding one or more lipid droplets often with internalized membrane fragments (3). The present study documents liver alteration after a short term single dose exposure to PCBs with high chlorine content, and correlates them with reported animal weights and central nervous system (CNS) measures. In the brain PCB congeners were concentrated in particular regions (4) while catecholamine concentrations were decreased (4-6). Urinary levels of homovanillic acid a dopamine metabolite were evaluated (7).Wistar rats were gavaged with corn oil (6 controls), or with a 1:1 mixture of Aroclor 1254 and 1260 in corn oil at 500 or 1000 mg total PCB/kg (6 at each level).

Potentiation of bromotrichloromethane hepatotoxicity in male rats exposed to 10 ppm dietary chlordecone: Electron Microscopic and biochemical study

1990 ◽  
Vol 48 (3) ◽  
pp. 284-285
Author(s):  
O. M. Faroon ◽  
R. W. Henry ◽  
M. G. Soni ◽  
H. M. Mehendale
Keyword(s):  
Free Radical ◽  
Biochemical Study ◽  
Prior Exposure ◽  
Male Rats ◽  
Cellular Injury ◽  
Low Doses ◽  
Mixed Function Oxidase ◽  
Electron Microscopic ◽  
Potent Inducer ◽  
Cellular Energy

Previous work has shown that mirex undergoes photolytic dechlorination to chlordecone (CD) (KeponeR) in the environment. Much work has shown that prior exposure to nontoxic levels of CD causes potentiation of hepatotoxicity and lethality of CCl4, BrCCl3 and other halomethane compounds. Potentiation of bromotrichloromethane hepatotoxicity has been associated with compounds that stimulate the activity of hepatic mixed-function oxidase (MFO). An increase in the metabolism of halomethane by the MFO to a free radical initiates peroxidative decomposition of membranal lipids ending in massive cellular injury. However, not all MFO inducers potentiate BrCCl3 hepatotoxicity. Potentiation by much larger doses of phenobarbital is minimal and th at by a more potent inducer of MFO, mirex, is negligible at low doses. We suggest that the CD and bromotrichloromethane interaction results in a depletion of cellular energy and thereby reducing the cellular ability to undergo mitosis.

Sign in / Sign up

Export Citation Format

Share Document