ABSTRACT
The present study examines the effects of early simultaneous exposure to low level of lead and cadmium on anxiety-like behaviour in the rat, and on monoamine levels in the hypothalamus and hippocampus at weaning and adult animals. Rats were intoxicated with cadmium acetate (10 mg/l) and lead acetate (300 mg/l) in drinking water from the beginning of pregnancy until weaning. Maternal co-exposure to lead and cadmium produced mainly alterations in dopaminergic and serotoninergic systems of hippocampus in both age studied, while noradrenaline content in hypothalamus and hippocampus remained unchanged at 75 days of age. The intoxicated rats showed an increased on indices of anxiety on the elevated plus-maze. These long-term changes in anxiety-like behaviour can be related to dopaminergic and serotoninergic alterations detected in hippocampus.
Subject(s)
Acetates/toxicity , Anxiety/chemically induced , Behavior, Animal/drug effects , Cadmium/toxicity , Organometallic Compounds/toxicity , Prenatal Exposure Delayed Effects , Animals , Biogenic Monoamines/metabolism , Female , Hippocampus/drug effects , Hippocampus/metabolism , Hypothalamus/drug effects , Hypothalamus/metabolism , Lactation , Male , Maze Learning/drug effects , Pregnancy , Rats , Rats, WistarABSTRACT
The present study was designed to examine more fully the neurochemical and behavioral interactions that derive from continued lead and cadmium poisoning in pups, whose mothers were exposed via drinking water (300 mg/l of Pb and 10 mg/l of Cd) throughout pregnancy and lactation. At weaning, these metals produced an increase in DOPAC, 5-HT and 5-HIAA contents in cerebellum, but the monoamine contents in striatum remained unaltered. The cerebral energetic metabolism was modified by the Cd-Pb exposition only in striatum. On the other hand, the Na+/K+-ATPase activity was inhibited significantly in both regions at PN21, whereas the alkaline phosphatase activity was not affected by the treatment. The intoxicated animals showed a short-term normocitic anemia, but revealed long-term alterations in the motor activity in open-field, where they showed an increase in both ambulating and rearing. So, it can be concluded that perinatal exposure to lead and cadmium provoke neurochemical alterations in cerebellum and striatum that can be related with the changes in motor activity observed in the adulthood.
Subject(s)
Abnormalities, Drug-Induced , Cadmium/toxicity , Cerebellum/drug effects , Corpus Striatum/drug effects , Lead/toxicity , Prenatal Exposure Delayed Effects , Teratogens/toxicity , 3,4-Dihydroxyphenylacetic Acid/metabolism , Animals , Animals, Newborn , Cadmium/administration & dosage , Cerebellum/metabolism , Corpus Striatum/metabolism , Drinking , Drug Combinations , Exploratory Behavior/drug effects , Female , Hydroxyindoleacetic Acid/metabolism , Lactation , Lead/administration & dosage , Male , Organ Size/drug effects , Pregnancy , Rats , Rats, Wistar , Serotonin/metabolism , Sodium-Potassium-Exchanging ATPase/antagonists & inhibitors , Sodium-Potassium-Exchanging ATPase/metabolism , Weight Gain/drug effectsABSTRACT
The effects of lead (Pb) intoxication during pregnancy and lactation were studied in the hepatic system of pups and young Wistar rats to test the hypothesis that gestational and lactational lead exposure alters the normal function of the liver in neonates. Lead acetate (300 mg/L) dissolved in distilled water was administered ad libitum to mothers during gestation and lactation. At days 12 and 21 postnatal (PN), pups were sacrificed, blood was collected, and livers were removed. Blood lead (PbB) levels were also measured. Although, histological evaluation revealed neither abnormalities in the liver structure nor depositions of lead, the toxicant produced biochemical alterations. Lead-intoxicated pups exhibited a decrease in hemoglobin, iron, and alkaline and acid phosphatase levels and an increase in PbB content. Protein, DNA, and lipid total amounts were reduced, and hepatic glycogen content was diminished at days 12 and 21 PN, with a higher level of glucose in the blood. Lead administration also resulted in a decrease in alkaline phosphatase in the liver of pups at day 21 PN, but acid phosphatase was unaltered. The findings of this study support the hypothesis that lead intoxication of mothers in gestation and lactation results in alterations in the hepatic system in neonates and pups.
