Embryotoxic and long-term effects of cadmium exposure during embryogenesis in rats

Salvatori, Francesca; Talassi, C.B; Salzgeber, S.A.; Spinosa, Helenice de Souza; Bernardi, Maria Martha

doi:10.1016/j.ntt.2004.05.001

Cited by 83 publications

(85 citation statements)

References 23 publications

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“…Importantly, exposure to Cd in utero did not impair fetus growth since the fetal weights and the craniocaudal length at the end of gestation (GD20) of the control and Cd group were not statistically different. This is in accordance with the study of Salvatori et al [35], who administered Cd at 20 mg/kg of body weight from GD 6 to GD 14. The Cd dose administered in the present study, considered as low [36], may explain the absence of toxicity in male fetus.…”

Section: Discussionsupporting

confidence: 93%

Protective role of zinc against the toxicity induced by exposure to cadmium during gestation and lactation on testis development

Chemek

Mimouna

Boughammoura

et al. 2016

Reproductive Toxicology

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Highlights Effects of Cd and Zn on testicular development were assessed. Cd accumulation and Zn depletion in testis during lactation were noted. Cd-induced abnormal seminiferous tubules and a plasmatic testosterone decrease. Zn supply induced a significant protection against Cd toxicity. Cd toxicity observed in pups is mediated by disruption of maternal Zn metabolism. *Research Highlights AbstractTo assess the effects of exposure to Cd and Zn on rat testicular development, offspring, from mothers receiving either tap water, Cd, Zn or Cd+Zn during gestation and lactation periods, were observed on gestational day (GD) 20 and on postnatal days (PND) 12, 21 and 35. During gestation, Cd induced maternal hypozincemia and less transfer of Zn to the fetus. During lactation, progressive Cd accumulation and Zn depletion in testis at PND12 and PND21 werenoted. An increase of abnormal seminiferous tubules and a decrease in testis weight and plasmatic testosterone concentration were also observed at PND21 and PND35 respectively. Interestingly, Zn supply induced a significant protection against Cd toxicity. These results suggest that the toxic effects of Cd observed during development are mediated by the disruption of Zn metabolism, which is established in mothers during pregnancy causing Zn deficiency in fetuses and continues to become more pronounced during lactation.

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Section: Discussionsupporting

confidence: 93%

Protective role of zinc against the toxicity induced by exposure to cadmium during gestation and lactation on testis development

Chemek

Mimouna

Boughammoura

et al. 2016

Reproductive Toxicology

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“…In experiments using perinatal exposure, changes in the mother, such as weight loss or changes in maternal homeostasis, may interfere indirectly with the development of offspring [30][31][32][33]. The nonoccurrence of maternal toxicity seen in present experiment indicates that any change occurring with the offspring' was therefore exclusively due to exposure to fipronil.…”

Section: Discussionmentioning

confidence: 56%

Lactational Exposure to Fipronil Pesticide in Low Dose Impairs Memory in Rat Offspring

Montanha¹,

Machado²

2016

J Neurol Disord

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Perinatal exposure to pesticides has been associated with neurotoxic changes that may occur during offspring development. This work aimed to evaluate the memory behavior in young and adult offspring from Wistar rats exposed to fipronil in the lactational period. For this, pregnant rats were distributed into two groups (N = 15) constituted as follows: control (Ct) and exposed to fipronil (Fip). Fipronil (Topline®) was administrated to mothers topically, at dose of 1 mg/kg/day, from the 7-14th day of lactation. The offspring memory behavior was assessed using the new object recognition task (ORT) and eight-radial arm maze task (8-RAM). Additionally was quantified the activity of the acetylcholinesterase enzyme (AChE) and made histopathological analysis of brain tissue. Results show persistent decreased memory behavior in offspring exposed to fipronil during lactation period associated with altered AChE activity and morphological changes in the animal's brain tissue. It is concluded that lactational exposure to fipronil provoked damage to the central nervous system (CNS) including altered memory behavior with histopathological and biochemical changes.

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“…In addition, the activity of some enzymes decreases, in particular, glutathione peroxidase, glutathione reductase, glucose-6-phosphatase, that can be a test for early diagnosis of damaged liver tissue (El-Shahat et al, 2009;Hariv and Gutyj, 2016). The peculiarity of the harmful effects of cadmium is its rapid absorption by the body and slow output, which leads to accumulation of the following metal in the tissues (Salvatori et al, 2004;Kumar and Prasad, 2004;Lu et al, 2005;Darmohray and Gonchar, 2015). Cadmium accumulates mainly in the liver and kidneys and has a long half-life (up to 30 years), mainly, in the aspect of the application it can be assumed that the deposition of cadmium in the animals' bodies is a lifetime.…”

Section: Resultsmentioning

confidence: 99%

Prooxidant-antioxidant balance in the organism of bulls (young cattle) after using cadmium load

Gutyj¹,

Stybel²,

Darmohray³

et al. 2017

Ukr J Ecol

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The results of studies of the effect of Cadmium influence on the state of the enzyme and nonenzyme system of antioxidant protection of young cattle organism, namely on the activity of superoxide dismutase, catalase, glutathione peroxidase, level of reduced glutathione, Selenium, vitamins A and E. It was determined that the feeding of young bulls with cadmium chloride in a dose of 0.04 mg / kg of body weight contributed to a decrease both, enzyme and non enzyme level of the system of antioxidant protection (superoxide dismutase by 22%, catalase -by 12%, renewed glutathione by 11%, glutathione peroxidase by 22 %, Selenium -by 18%, vitamin A -by 23%, vitamin E -by 27%,). The lowest level of the antioxidant protection system in the blood of young cattle was set at the sixteenth and twenty-fourth day of the experiment, which is due to the increased activation of lipoperoxidation processes and a disturbance of the balance between the activity of the antioxidant system and the intensity of peroxidation of lipids. The toxic effect of Cadmium contributes to the change in the stationary concentrations of the radical metabolites O2, ˙OH, NO2, which, in their turn, initiate the processes of peroxide oxidation of lipids, indicating an increase in the level of diene conjugates and malonic dialdehyde. The highest level of intermediate and final products of peroxid oxidation of lipids in the blood of young cattle was determined on the thirtieth day of the experiment, while comparing with the control group, they increased by 31 and 27%, respectively.

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Embryotoxic and long-term effects of cadmium exposure during embryogenesis in rats

Cited by 83 publications

References 23 publications

Protective role of zinc against the toxicity induced by exposure to cadmium during gestation and lactation on testis development

Protective role of zinc against the toxicity induced by exposure to cadmium during gestation and lactation on testis development

Lactational Exposure to Fipronil Pesticide in Low Dose Impairs Memory in Rat Offspring

Prooxidant-antioxidant balance in the organism of bulls (young cattle) after using cadmium load

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