Investigation of acute lead poisoning on apoptosis in rat hippocampus in vivo

Sharifi, Ali Mohammad; Baniasadi, Shadi; Jorjani, Masoumeh; Rahimi, Farzaneh; Bakhshayesh, Masoomeh

doi:10.1016/s0304-3940(02)00576-1

Cited by 91 publications

(41 citation statements)

References 14 publications

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“…Also, previous studies have shown that ALA is generated even in the brain 103,104) . We may therefore hypothesize that lead impairs children's intelligence and neurobehavioral performance, possibly due to increased ALA in the brain, despite the presence of at least one animal experiment reporting that lead-induced cell death in the hippocampus in vivo may be partly due to apoptosis 105) . However, this raises some questions: a) Can ALA at a low level truly damage the immature brain in infants?…”

Section: Lead Toxicity In Childrenmentioning

confidence: 99%

Lead Toxicity: Does the Critical Level of Lead Resulting in Adverse Effects Differ between Adults and Children?

Murata

Iwata

Dakeishi

et al. 2009

Journal of Occupational Health

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µg/dl for industrial workers and 5 µg/dl for children. To examine whether the critical level of lead producing adverse effects truly differs between workers and children, we provided an overview of studies addressing the critical level of lead in workers, together with a perspective on lead toxicity in children. Data sources and extraction: In 25 reports published in English with keywords of "benchmark dose (BMD)," "lead" and "humans," only five studies proved to be relevant to lead toxicity. Four more studies with figures illustrating significant relationships between lead and neurotoxic outcomes were selected. Data synthesis: Based on data from previous reports using a BMD approach, the critical organ of lead in workers was thought to be the nervous system and the critical BPb level (numberweighted mean) was between 10.7 and 17.5 µg/dl. The neurotoxic effects of lead exposure at such levels seemed reversible. The BPb level at which leadassociated intellectual deficits occurred in children was as low as the critical level of BPb (below 5 µg/dl) for inhibited heme synthesis in workers. Conclusions: The neurotoxic effects of lead in workers appear to be initiated at BPb levels below 18 µg/dl, which are somewhat higher than the critical level of lead neurotoxicity in children. Each national institute for risk Review management should take evidence-based preventive action against subclinical lead poisoning in workers, as well as in children. (J Occup Health 2009; 51: 1-12)

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Section: Lead Toxicity In Childrenmentioning

confidence: 99%

Lead Toxicity: Does the Critical Level of Lead Resulting in Adverse Effects Differ between Adults and Children?

Murata

Iwata

Dakeishi

et al. 2009

Journal of Occupational Health

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“…It has been shown that some exogenous chemicalinduced neurotoxicities may be associated with the facilitation of apoptosis in the hippocampus 22−25) . Lead (Pb) is a common neurotoxicant, and it was found to induce apoptosis in the hippocampus of experimental animals in vivo 25) . Some studies have shown that other neurotoxicants such as CuO, MnCl 2 and ethanol also induced hippocampal neural apoptosis in rats or mice 20,24,26) .…”

mentioning

confidence: 99%

Subchronic exposure to arsenic induces apoptosis in the hippocampus of the mouse brains through the Bcl‐2/Bax pathway

Wang

Bai

Guan

et al. 2015

Journal of Occupational Health

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were found in the hippocampus of As-exposed mice. The expressions of the Bcl-2 gene and its protein in the hippocampus of As-exposed mice were significantly lower than those in the control group (p<0.05). However, the expressions of the Bax gene and its protein, and the expression ratio of Bax/Bcl-2 in the hippocampus were significantly higher in the groups exposed to As than in the control group (p<0.05). Moreover, the activity of caspase-3 in the hippocampus of mice exposed to As was higher than that in the control (p<0.05). Conclusions:These results indicate that subchronic exposure to As induces apoptosis in the hippocampus of mice by disturbing normal Bax/Bcl-2 regulatory pathways. Meanwhile, it is suggested that the induced apoptosis in the hippocampus may be at least partly responsible for As-induced neurotoxicity. (J Occup Health 2015; 57: 212-221) Key words: Apoptosis, Arsenic trioxide, Bax, Bcl-2, Hippocampus, Neurotoxicity Arsenic (As), a naturally occurring toxic metalloid found in both inorganic and organic forms, is ubiquitous in the environment and contaminates water as a result of geological and industrial pollution 1) . Moreover, some kinds of arsenide, such as arsenic trioxide (As 2 O 3 ), are also widely used for the treatment of malignant tumors 2) . In As-contaminated areas, the As concentration in drinking water or groundwater ranges from 0.25 to 2.1 ppm and even reaches >3.0 ppm in some severely contaminated areas 3−5) . Exposure to As has been associated with increasing incidences of various chronic diseases, including peripheral vascular disease, cardiovascular disease, diabetes mellitus, and various cancers 6) . As is also a potent neurotoxicant, and subchronic or chronic As exposure causes severe nervous system Abstract: Subchronic exposure to arsenic induces apoptosis in the hippocampus of the mouse brains through the Bcl-2/Bax pathway: Yachen WANG, et al. Department of Occupational and EnvironmentalHealth, Dalian Medical University, P.R. ChinaObjectives: The aim of this study was to identify whether arsenic (As) exposure could induce hippocampal neural apoptosis in vivo. Methods: Sixty-four mice were randomly divided into 4 groups of 16 each. Group 1 orally received drinking water alone as a control. Groups 2−4 were given arsenic trioxide (As 2 O 3 ) orally at the doses of 1 ppm, 2 ppm and 4 ppm, respectively. All the treatments continued for 60 days. Morphological changes in the hippocampus were observed by HE staining. Apoptosis in the hippocampus was examined by TUNEL assay and transmission electron microscopy. The expression levels of Bcl-2 and Bax genes and their proteins in the hippocampus were determined by realtime PCR and Western blotting. The activity of caspase-3 was determined by spectrophotometry. Results: Abnormal histopathological changes and apoptosis

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“…Although the mechanisms of ROS-induced apoptosis are not fully understood, the role of signaling pathways, including lipid messengers or lipid peroxide, might be involved in lead-induced apoptosis (Maccarone and Catani, 1997;Morel and Barouki, 1999;Nagata, 1997;Sarafian and Bredesen, 1994). In a recent study, Sharifi et al has shown that lead-induced cell death in rat hippocampus in vivo is due to apoptosis (Sharifi et al, 2002). The results obtained from the caspase-3 assay indicated that 500 μM of lead acetate exposure induced apoptosis in PC-12 cells.…”

Section: Discussionmentioning

confidence: 99%

Effects of selenocystine on lead-exposed Chinese hamster ovary (CHO) and PC-12 cells

Aykin-Burns

Erçal

2006

Toxicology and Applied Pharmacology

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Lead is a pervasive environmental toxin that affects multiple organ systems, including the nervous, renal, reproductive, and hematological systems. Even though it is probably the most studied toxic metal, some of the symptoms of lead toxicity still cannot be explained by known molecular mechanisms. Therefore, lead-induced oxidative stress has recently started to gain attention. This in vitro study confirms the existence of oxidative stress due to lead exposure. Administration of lead acetate (PbA) to cultures of Chinese hamster ovary cells (CHO) had a concentrationdependent inhibitory effect on colony formation and cell proliferation. This inhibition was eliminated by 5 μM selenocystine (SeCys). In order to evaluate the nature of SeCys's effect, we measured glutathione (GSH), its oxidized form glutathione disulfide (GSSG), malondialdehyde (MDA), catalase, and GSH peroxidase (GPx) activities in lead-exposed CHO cells both in the presence and absence of SeCys. Increases in MDA, catalase, and GPx activities were observed in cultures that received only PbA, but supplementation with SeCys returned these measures to pretreatment levels. The ratio of GSH to GSSG increased in lead-exposed cells incubated in SeCys-enhanced media but declined in cultures treated with PbA only. In order to determine whether SeCys also reverses lead-induced neurotoxicity, a neuronal cell line, PC-12 cells, was used. Lead's inhibition on neurite formation was significantly eliminated by SeCys in PC-12 cells. Our results suggest that SeCys can confer protection against leadinduced toxicity in CHO cells and neurotoxicity in PC-12 cells.

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Investigation of acute lead poisoning on apoptosis in rat hippocampus in vivo

Cited by 91 publications

References 14 publications

Lead Toxicity: Does the Critical Level of Lead Resulting in Adverse Effects Differ between Adults and Children?

Lead Toxicity: Does the Critical Level of Lead Resulting in Adverse Effects Differ between Adults and Children?

Subchronic exposure to arsenic induces apoptosis in the hippocampus of the mouse brains through the Bcl‐2/Bax pathway

Effects of selenocystine on lead-exposed Chinese hamster ovary (CHO) and PC-12 cells

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