Protein malnourishment: a predisposing factor in acrylamide toxicity in pregnant rats.
Exposure to acrylamide (3-10 mg/kg body weight) was found to be lethal for protein-deficient pregnant rats as evidenced by their increased mortality. It had no such effect on the normal protein diet fed pregnant and nonpregnant rats and the protein-malnourished nonpregnant rats. Protein deficiency during pregnancy caused a significant decrease in the activity of brain monoamine oxidase and acetylcholinesterase and striatal [3H]spiperone binding, known to label dopamine receptors; had no significant effect on the binding of 3H-QNB (quinuclidinyl benzilate) to cerebellar and [3H]diazepam to frontocortical membranes, known to label muscarinic and benzodiazepine receptors, respectively; and had no significant effect on brain glutathione (GSH) levels in comparison with pregnant rats fed normal protein diet. Exposure to acrylamide (2 mg/kg body weight) in protein-malnourished pregnant rats caused a marked decrease in the activity of monoamine oxidase and acetylcholinesterase and also in the binding of [3H]spiperone, [3H]QNB, and [3H]diazepam to striatal, cerebellar, and frontocortical membranes, respectively. Kinetic studies revealed that decreased binding of these ligands in the specific brain regions were due to decreased receptor sites (Bmax). A reduction in the brain glutathione content was also observed in these animals in comparison with those fed a low-protein diet during pregnancy. Pregnant rats fed a normal-protein diet on acrylamide exposure, however, showed no such biochemical changes in comparison with the pregnant rats fed normal protein diet. Also, no effect on any of the parameters studied was observed in the adult nonpregnant rats fed a low-protein diet (for 18 d) and those exposed to the monomer (d 6-17) fed either a normal- or low-protein diet in comparison with respective controls. The results indicate that pregnancy under conditions of malnutrition modifies the susceptibility of pregnant rats toward acrylamide.
Khanna
V K
VK
Industrial Toxicology Research Centre, Lucknow, India.
Husain
R
R
Seth
P K
PK
D000110:Acetylcholinesterase / Q000187:drug effects / Q000378:metabolism; D020106:Acrylamide; D000178:Acrylamides / Q000633:toxicity*; D000818:Animals; D001835:Body Weight / Q000187:drug effects; D001927:Brain Diseases / Q000139:chemically induced / Q000201:enzymology / Q000378:metabolism; D005260:Female; D005978:Glutathione / Q000378:metabolism; D008297:Male; D008995:Monoamine Oxidase / Q000187:drug effects / Q000378:metabolism; D009929:Organ Size / Q000187:drug effects; D011247:Pregnancy; D011248:Pregnancy Complications / Q000201:enzymology / Q000378:metabolism*; D011270:Pregnancy, Animal / Q000187:drug effects* / Q000378:metabolism; D011502:Protein-Energy Malnutrition / Q000201:enzymology / Q000378:metabolism / Q000503:physiopathology*; D051381:Rats; D011919:Rats, Inbred Strains; D017981:Receptors, Neurotransmitter / Q000187:drug effects / Q000378:metabolism
D000178:Acrylamides; D017981:Receptors, Neurotransmitter; D020106:Acrylamide; D008995:Monoamine Oxidase; D000110:Acetylcholinesterase; D005978:Glutathione