Effects of lead and/or zinc exposure during the second stage of rapid postnatal brain growth on delta-aminolevulinate dehydratase and negative geotaxis of suckling rats

Goulart, E.C.; Pereira, C.; Garcia, R.C.; Giacomelli, Maria Bertı́lia Oss; Rodrigues, Ana Lúcia S.

doi:10.1590/s0100-879x2001000600014

Cited by 11 publications

(5 citation statements)

References 17 publications

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“…[95][96][97] The stimulation of δ-ALA-D synthesis after Pb(II) intoxication was interpreted as a compensatory response to the enzyme inhibition. We have observed that a short-term exposure of suckling rats to high doses of Pb(II) caused an increase in blood δ-ALA-D activity 35 and an increase in the reactivation index by dithiothreitol (DTT) + Zn(II) of two times, 98 corroborating the findings of Fujita and collaborators. [95][96][97] In contrast to rats, workers from battery manufacturing plants exposed to lead exhibited an increase in δ-ALA-D gene methylation and a decrease in δ-ALA-D transcription.…”

Section: Pb(ii) In Vivosupporting

confidence: 88%

Aminolevulinate dehydratase (δ-ALA-D) as marker protein of intoxication with metals and other pro-oxidant situations

et al. 2012

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δ-ALA-D is a metalloenzyme that has 3 vicinal thiol/thiolate groups that coordinate with Zn(II). The proximity between the sulfhydryl groups renders δ-ALA-D extremely sensitive to oxidation by soft electrophiles, such as Pb(II), Hg(II), As(III) and organoseleno and organotellurium compounds. In fact, blood δ-ALA-D is a classical biomarker of lead exposure in humans. The inhibition of δ-ALA-D can increase the concentration of 5-aminolevulinate (δ-ALA), which is a pro-oxidant compound. δ-ALA can generate oxidative stress that can further increase δ-ALA-D inhibition. Recently, data have been obtained indicating that the δ-ALA-D could be a marker of oxidative stress in human pathologies. In summary, considering its high sensitivity to pro-oxidant situations, δ-ALA-D can be considered a universal marker of oxidative stress.

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Section: Pb(ii) In Vivosupporting

confidence: 88%

Aminolevulinate dehydratase (δ-ALA-D) as marker protein of intoxication with metals and other pro-oxidant situations

et al. 2012

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“…These results are in accordance with several preceding studies [9,37,48,72,73] that reported similar findings of neuronal degeneration in Pb and other heavy metal toxicity on the cerebellums, with more consequences for the Purkinje cells due to sensitivity of the Purkinje cell layer. Further, previous studies also documented the toxic effect of Pb administration on juvenile and young rats, resulting in different neurological impairments in various parts of the brain and nervous system [74,75,76,77]. However, treatment with curcumin reversed the above-mentioned Pb-induced morphological aberrations in the rats.…”

Section: Discussionmentioning

confidence: 92%

Curcumin Attenuates Lead-Induced Cerebellar Toxicity in Rats via Chelating Activity and Inhibition of Oxidative Stress

et al. 2019

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Lead (Pb) is a toxic, environmental heavy metal that induces serious clinical defects in all organs, with the nervous system being its primary target. Curcumin is the main active constituent of turmeric rhizome (Curcuma longa) with strong antioxidant and anti-inflammatory properties. This study is aimed at evaluating the therapeutic potentials of curcumin on Pb-induced neurotoxicity. Thirty-six male Sprague Dawley rats were randomly assigned into five groups with 12 rats in the control (normal saline) and 6 rats in each of groups, i.e., the lead-treated group (LTG) (50 mg/kg lead acetate for four weeks), recovery group (RC) (50 mg/kg lead acetate for four weeks), treatment group 1 (Cur100) (50 mg/kg lead acetate for four weeks, followed by 100 mg/kg curcumin for four weeks) and treatment group 2 (Cur200) (50 mg/kg lead acetate for four weeks, followed by 200 mg/kg curcumin for four weeks). All experimental groups received oral treatment via orogastric tube on alternate days. Motor function was assessed using a horizontal bar method. The cerebellar concentration of Pb was evaluated using ICP-MS technique. Pb-administered rats showed a significant decrease in motor scores and Superoxide Dismutase (SOD) activity with increased Malondialdehyde (MDA) levels. In addition, a marked increase in cerebellar Pb concentration and alterations in the histological architecture of the cerebellar cortex layers were recorded. However, treatment with curcumin improved the motor score, reduced Pb concentration in the cerebellum, and ameliorated the markers of oxidative stress, as well as restored the histological architecture of the cerebellum. The results of this study suggest that curcumin attenuates Pb-induced neurotoxicity via inhibition of oxidative stress and chelating activity.

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“…Test pups were placed head down on the rough surface and allowed to turn 180° within 60 s [9] . The pups were tested for negative geotaxis on days 8, 10 and 12 of age.…”

Section: Negative Geotaxismentioning

confidence: 99%

Developmental and Behavioral Consequences of Prenatal Fluoxetine

Bairy¹,

Madhyastha²,

Ashok

et al. 2006

Pharmacology

103

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Background: Fluoxetine, a selective serotonin reuptake inhibitor, is the most commonly prescribed antidepressant drug for pregnant women. Studies regarding the teratogenic effect of fluoxetine on human and animal models are mainly concerned with structural malformation (congenital anomalies). Aim: Hence, the present study was planned to evaluate the postnatal behavioral effects of fluoxetine on albino rats. Methods: Three groups of female rats received either distilled water or doses of fluoxetine 8 and 12 mg/kg orally from the 6th to the 20th day of pregnancy. Weaning of the pups was done on the 21st day followed by a battery of behavioral tests to assess for any behavioral effect. The tests included negative geotaxis, open field exploration, rota-rod test, elevated plus maze and passive avoidance test. Results: In the present study there was no change in the gestational length of pregnancy, no premature birth or miscarriage during pregnancy. A high dose of in utero fluoxetine resulted in a decrease in birth weight of the offspring and also reduced weight gain during the preweaning period. No major congenital abnormalities were observed in the offspring exposed to fluoxetine. Prenatal fluoxetine exposure at high dose caused an initial transient delay in motor development and this poor motor activity was transient and not permanent. However, prenatal exposure to fluoxetine at a higher dose showed a favorable effect on learning and memory in water maze and passive avoidance tests. Conclusions: From the present study, it may be concluded that prenatal fluoxetine causes a transient delay in motor development but does not adversely affect the postnatal behavioral consequences.

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Effects of lead and/or zinc exposure during the second stage of rapid postnatal brain growth on delta-aminolevulinate dehydratase and negative geotaxis of suckling rats

Cited by 11 publications

References 17 publications

Aminolevulinate dehydratase (δ-ALA-D) as marker protein of intoxication with metals and other pro-oxidant situations

Aminolevulinate dehydratase (δ-ALA-D) as marker protein of intoxication with metals and other pro-oxidant situations

Curcumin Attenuates Lead-Induced Cerebellar Toxicity in Rats via Chelating Activity and Inhibition of Oxidative Stress

Developmental and Behavioral Consequences of Prenatal Fluoxetine

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