Arsenic, cadmium and lead

Flora, S.J.S.; Pachauri, Vidhu; Saxena, Geetu

doi:10.1016/b978-0-12-382032-7.10033-5

Cited by 47 publications

(29 citation statements)

References 129 publications

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“…6,9 The reproductive system can also be affected, resulting in decreased reproductive success through abnormal spermatogenesis, decreased fertility in females, fetal development abnormalities, miscarriage, premature membrane rupture and preeclampsia, as well as a delay in fetal growth and postnatal neurotoxic effects. [10][11][12] The Tasmanian devil, Sarcophilus harrisii, is the largest marsupial carnivore remaining in Tasmania since the last thylacine (Thylacinus cynocephalus) died in the 1930s. 13 Tasmanian devils are the focus of intense conservation efforts and are listed as 'Endangered' on the International Union for Conservation of Nature's Red List 14 in view of the dramatic decrease of their population since the appearance of devil facial tumour disease (DFTD), a contagious cancer associated with high mortality.…”

Section: Methodsmentioning

confidence: 99%

High blood lead concentrations in captive Tasmanian devils (Sarcophilus harrisii): a threat to the conservation of the species?

et al. 2018

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Background The Tasmanian devil (Sarcophilus harrisii) is the world’s largest extant marsupial carnivore. Since the emergence of devil facial tumour disease in 1996, the species has undergone a severe population decline. The insurance population (IP) was established in 2006 to build a disease‐free captive population to maintain 95% of the wild Tasmanian devil genetic diversity for 50 years. Captive and semi‐wild Tasmanian devils are fed with possum and wallaby meat provided by local hunters, who use lead ammunition. Lead ingestion can cause acute toxicity, including ataxia, coma and death, or chronic subclinical deleterious effects including decreased fertility. Methods We determined blood lead concentrations in 26 captive and 133 wild Tasmanian devils from various sites across Tasmania. Results Captive Tasmanian devils showed significantly higher blood lead concentrations than their conspecifics in the wild. In captivity, older animals had higher blood lead concentrations than young animals, which suggested regular exposure, as lead can accumulate in a living organism in the blood, soft tissues and bones. After a response measure was implemented by removing the heads and wounds containing lead from the diet, blood concentrations significantly decreased in animals at one of the captive study sites, supporting the suspicion of food as the source of lead. Conclusion This study highlights the need to ensure meat fed to captive carnivores is not contaminated by lead, especially in the context of a conservation program breeding individuals in captivity, as for Tasmanian devils.

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Section: Methodsmentioning

confidence: 99%

High blood lead concentrations in captive Tasmanian devils (Sarcophilus harrisii): a threat to the conservation of the species?

et al. 2018

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“…Lead is known to induce a broad range of physiological, biochemical, histological and behavioral dysfunctions in laboratory animals and humans including nervous system (Flora et al, 2006), kidneys (Rastogi, 2008), liver (Kasten-Jolly et al, 2010), male and female reproductive systems (Flora et al, 2011). Its negative impact on reproduction is well known (Alexander et al, 1996;Gandley et al, 1999;Bonde et al, 2002).…”

Section: Introductionmentioning

confidence: 98%

The ameliorative effects of DMSA and some vitamins against toxicity induced by lead in the testes of albino rats. II

El-Sayed

Abdel-Ghafar

Adly

et al. 2015

The Journal of Basic & Applied Zoology

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Lead is a poison that affects virtually every system in the body. The current study was planned to examine the toxic effects of lead acetate on the histological picture of testes, and the protective roles of DMSA, combined vitamins C and E, and DMSA combined with vitamin C plus vitamin E against the histopathological changes in the testes of albino rats induced by lead acetate. Oral administration of lead acetate caused necrosis of spermatogenic cells in the seminiferous tubules, congestion of interstitial blood vessels, severe interstitial edema and complete necrosis in the seminiferous tubules. Co-administration of DMSA with lead acetate minimized the histopathological changes exhibited by lead acetate in the affected organ compared with lead acetateintoxicated rats. Lead acetate combined with vitamin C plus vitamin E supplemented rats showed mild congestion of the interstitial blood vessels and the seminiferous tubules with its components appeared normal compared to DMSA treated rats. Treatment with DMSA combined with vitamin C plus vitamin E showed more or less normal histological appearance of the testes in lead acetate induced histopathological changes in the affected organ. These results show that DMSA, as a chelating agent for lead, and the combination of vitamins C and E as antioxidants reduced the toxic effects of lead on the histological structure of testes in albino rats but did not provide complete protection. Whereas, the supplementation of DMSA combined with both vitamins C and E provide complete protection against toxicity induced by lead in the testes of albino rats. ª 2015 The Egyptian German Society for Zoology. Production and hosting by Elsevier B.V. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

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“…It is noted that this inhibitory concentration is comparable to blood lead levels (40.0 ± 16.5 μg/dL, mean ± SD) in a certain proportion of pregnant women (Ugwuja et al 2013). Although lead caused craniofacial malformations only in cultured rat embryos (Zhao et al 1997) and does not cause major malformations in humans, its migration-inhibitory effects on cNCCs, as a neuronal progenitor, may be related to functional deficiencies such as neurological alterations (Flora et al 2011). The effects of the two selenium compounds on the migration of cNCCs were different in the present study; i.e., selenate inhibited the migration of cNCCs while selenite did not.…”

Section: Discussionmentioning

confidence: 95%

Effects of 13 developmentally toxic chemicals on the migration of rat cephalic neural crest cells in vitro

Usami

Mitsunaga

Miyajima

et al. 2016

Congenital Anomalies

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The inhibition of neural crest cell (NCC) migration has been considered as a possible pathogenic mechanism underlying chemical developmental toxicity. In this study, we examined the effects of 13 developmentally toxic chemicals on the migration of rat cephalic NCCs (cNCCs) by using a simple in vitro assay. cNCCs were cultured for 48 h as emigrants from rhombencephalic neural tubes explanted from rat embryos at day 10.5 of gestation. The chemicals were added to the culture medium at 24 h of culture. Migration of cNCCs was measured as the change in the radius (radius ratio) calculated from the circular spread of cNCCs between 24 and 48 h of culture. Of the chemicals examined, 13-cis-retinoic acid, ethanol, ibuprofen, lead acetate, salicylic acid, and selenate inhibited the migration of cNCCs at their embryotoxic concentrations; no effects were observed for acetaminophen, caffeine, indium, phenytoin, selenite, tributyltin, and valproic acid. In a cNCC proliferation assay, ethanol, ibuprofen, salicylic acid, selenate, and tributyltin inhibited cell proliferation, suggesting the contribution of the reduced cell number to the inhibited migration of cNCCs. It was determined that several developmentally toxic chemicals inhibited the migration of cNCCs, the effects of which were manifested as various craniofacial abnormalities.

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Arsenic, cadmium and lead

Cited by 47 publications

References 129 publications

High blood lead concentrations in captive Tasmanian devils (Sarcophilus harrisii): a threat to the conservation of the species?

High blood lead concentrations in captive Tasmanian devils (Sarcophilus harrisii): a threat to the conservation of the species?

The ameliorative effects of DMSA and some vitamins against toxicity induced by lead in the testes of albino rats. II

Effects of 13 developmentally toxic chemicals on the migration of rat cephalic neural crest cells in vitro

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