Maternal lead exposure and pregnancy outcome in Wistar albino rats

Aprioku, S.

doi:10.5897/jtehs2013.0279

Cited by 14 publications

(12 citation statements)

References 42 publications

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“…Two weeks after a recurrent i.p. administration of 10 mg/kg of lead acetate, the treated rats showed an inhibitory effect on body weight gain and a reduced ability of rate of growth as previously reported in lead-treated pregnant rats and pups (Aprioku and Siminialayi, 2013 ). This effect could be attributed, at least in part, to a deficiency in energy metabolism and to the alterations of normal cell metabolism (Patel et al, 1974 ; Wapnir et al, 1977 ).…”

Section: Discussionsupporting

confidence: 83%

Lead-Induced Atypical Parkinsonism in Rats: Behavioral, Electrophysiological, and Neurochemical Evidence for a Role of Noradrenaline Depletion

et al. 2018

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Background: Lead neurotoxicity is a major health problem known as a risk factor for neurodegenerative diseases, including the manifestation of parkinsonism-like disorder. While lead is known to preferentially accumulate in basal ganglia, the mechanisms underlying behavioral disorders remain unknown. Here, we investigated the neurophysiological and biochemical correlates of motor deficits induced by sub-chronic injections of lead.Methods: Sprague Dawely rats were exposed to sub-chronic injections of lead (10 mg/kg, i.p.) or to a single i.p. injection of 50 mg/kg N-(2-chloroethyl)-N-ethyl-2-bromobenzylamine hydrochloride (DSP-4), a drug known to induce selective depletion of noradrenaline. Rats were submitted to a battery of behavioral tests, including the open field for locomotor activity and rotarod for motor coordination. Electrophysiological recordings were carried out in three major basal ganglia nuclei, the subthalamic nucleus (STN), globus pallidus (GP), and substantia nigra pars reticulata (SNr). At the end of experiments, post-mortem tissue level of the three monoamines (dopamine, noradrenaline, and serotonin) and their metabolites has been determined using HPLC.Results: Lead intoxication significantly impaired exploratory and locomotor activity as well as motor coordination. It resulted in a significant reduction in the level of noradrenaline in the cortex and dopamine and its metabolites, DOPAC, and HVA, in the striatum. The tissue level of serotonin and its metabolite 5-HIAA was not affected in the two structures. Similarly, DSP-4, which induced a selective depletion of noradrenaline, significantly decreased exploratory, and locomotor activity as well as motor coordination. L-DOPA treatment did not improve motor deficits induced by lead and DSP-4 in the two animal groups. Electrophysiological recordings showed that both lead and DSP-4 did not change the firing rate but resulted in a switch from the regular normal firing to irregular and bursty discharge patterns of STN neurons. Neither lead nor DSP-4 treatments changed the firing rate and the pattern of GP and SNr neurons.Conclusions: Our findings provide evidence that lead represents a risk factor for inducing parkinsonism-like deficits. As the motor deficits induced by lead were not improved by L-DOPA, we suggest that the deficits may be due to the depletion of noradrenaline and the parallel disorganization of STN neuronal activity.

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Section: Discussionsupporting

confidence: 83%

Lead-Induced Atypical Parkinsonism in Rats: Behavioral, Electrophysiological, and Neurochemical Evidence for a Role of Noradrenaline Depletion

et al. 2018

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“…Another possible explanation for the loss of body weight may be decreased muscle mass and cachexia due to the oxidative stress induced by lead (Zaheer et al, 2013). Aprioku and Siminialayi (2013) reported significant and time-dependent reductions in body weight after perinatal exposure to 4 or 8 mg/kg lead acetate respectively. The result from the present study is dissimilar to the findings of Lewis and Pitts (2004) who reported an insignificant decrease in body weight of Wistar rat pups after 3-week post-natal exposure to lead acetate at (50, or 250 ppm) when compared with the control.…”

Section: Discussionmentioning

confidence: 98%

Assessment of the effect of post-natal lead exposure on the hippocampus of developing Wistar rats

2019

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This study examined the effect of post-natal lead exposure on the hippocampus of developing Wistar rats. Nine pregnant Wistar rats were randomly distributed into three groups of three rats each, consisting of a control Group 1 which received distilled water and experimental Groups 2 and 3 orally administered with 60 and 90 mg/kg bwt of lead acetate, respectively. The pups of the experimental Groups 2 and 3 were exposed to lead acetate via lactation from dams that were administered lead acetate from post-natal day (PND) 1 -PND 21. On PND 22, all the pups were weighed, and then euthanized. The brains of the pups were excised, weighed; lead deposit was quantified and fixed in Bouin's fluid. The results revealed a significant (p<0.05) decrease in body weight, insignificant (p>0.05) decrease in brain weight, significant increase(p<0.05) in brain somatic index (BSI), significant increase(p<0.05) in lead deposition, weak staining for Nissl substance and distortion in cytoarchitecture of the hippocampus of Wistar rat's pups exposed to lead acetate compared to the control. Post-natal exposure to lead acetate via lactation caused an increase in lead deposition, decrease in body weight and distortion in the cytoarchitecture of the hippocampus of developing Wistar rats.

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“…All these are serious negative indices of pregnancy, which can independently affect the overall wellbeing of the developing embryo or fetus. [ 18 19 20 ] Implantation of the embryo follows egg fertilization and is essential for embryo development and sustenance of pregnancy. The presence of implantations was observed only in 2 (25%) of the rats that received 800 mg/kg, whereas implantations were retained in six animals (75%) that were administered 400 mg/kg of Calabash chalk.…”

Section: Discussionmentioning

confidence: 99%