Determination of Optimal Toxic Concentration and Accumulation of Cadmium in Broiler Chicks

Subhan, Fazli; Khan, Ayaz Ali; Wahid, Fazli; Shehzad, Adeeb; Jan, Amin Ullah

doi:10.5487/tr.2011.27.3.143

Cited by 9 publications

(2 citation statements)

References 15 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Whereas group C received daily doses of Cd (75 mg /kg BW) + coral fossil（1 gm /kg BW) orally. The dose of cadmium and coral fossil were selected according to the study by Subhan et al (2011) and Xu et al, 2020a , Xu et al, 2020b . Both the Cd and coral fossil were given with water.…”

Section: Methodsmentioning

confidence: 99%

Coral fossil: A potential adsorbent of natural source for cadmium removal in broilers

Mustari

Alam

Khatun

et al. 2023

Saudi Journal of Biological Sciences

View full text Add to dashboard Cite

Section: Methodsmentioning

confidence: 99%

Coral fossil: A potential adsorbent of natural source for cadmium removal in broilers

Mustari

Alam

Khatun

et al. 2023

Saudi Journal of Biological Sciences

View full text Add to dashboard Cite

“…Groups III, IV, and V were fed basal diet containing CdCl 2 at 37.5, 75, and 150 mg/kg diet, respectively, and were gavaged with sunflower oil at 1.1 mL/kg/day. These CdCl 2 doses were previously used for toxicological studies in chickens ( 26 , 27 ). Groups VI, VII, and VIII were fed basal diet plus CdCl 2 at the above-mentioned consecutive doses and were administered orally BISA (50 mg/kg/day).…”

Section: Methodsmentioning

confidence: 99%

Antagonism of cadmium-induced liver injury in ducks by α-bisabolol

Elazab

Hsu

2022

Front. Vet. Sci.

View full text Add to dashboard Cite

Cadmium (Cd) is an ecological pollutant which causes hazardous effects in animals and humans. The aim of this study was to investigate the role of α-bisabolol (BISA) in antagonizing the Cd-induced hepatotoxicity in ducks. Two-week old ducks were allocated into 8 groups (10 ducks/group): Group I received basal diet and was gavaged with sunflower oil (BISA vehicle, 1.1 mL/kg/day); group II was administered BISA orally (50 mg/kg/day; diluted with sunflower oil); groups III, IV, and V were fed the basal diet mixed with CdCl2 at 37.5, 75, and 150 mg/kg diet, respectively, and were gavaged with sunflower oil; group VI, VII, and VIII were given basal diet containing CdCl2 at the aforementioned consecutive doses plus BISA. All treatments were provided daily for 4 weeks. Exposure to CdCl2 induced mortality in ducks, increased hepatic Cd content and serum levels of hepatopathic biomarkers, and caused oxidative stress and morphological alterations in ducks' liver. Furthermore, exposure to Cd caused upregulation of the mRNA of proinflammatory cytokine tumor necrosis factor-α and apoptotic gene Bax, and that of cyclooxygenase-2 protein in the liver. All effects of Cd were dose-dependent. BISA antagonized all of the aforementioned CdCl2-induced changes. These findings suggested that BISA exert the hepatoprotective effect against Cd toxicity through reducing the hepatic content of Cd as well as antagonizing oxidative insults, inflammation, and apoptosis. Thus, BISA has a great potential to be used as an antidote in the control of Cd poisoning.

show abstract

The Effect of Selenium on the Cd-Induced Apoptosis via NO-Mediated Mitochondrial Apoptosis Pathway in Chicken Liver

Zhang

et al. 2017

Biol Trace Elem Res

View full text Add to dashboard Cite

Cd-induced apoptosis and the protective effects of Se against Cd-induced injury have been reported in previous studies. However, little is known regarding the effects of Cd-induced apoptosis in hepatic cells and the antagonistic effects of Se on Cd in poultry. In the present study, 128 healthy 31-week-old laying hens were randomly divided into four groups, which were fed basic diets, with the addition of Se (NaSeO, 2 mg/kg), Cd (CdCl, 150 mg/kg), or Se + Cd (150 mg/kg of CdCl and 2 mg/kg of NaSeO) for 90 days. Ultrastructural changes, nitric oxide (NO) concentrations, inducible nitric oxide synthase (iNOS) activities, results of the terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay of apoptosis, and the expression of iNOS and apoptosis-related genes in livers were determined. It was observed that Cd treatment significantly increased the concentrations of NO and iNOS activity in chicken livers. The production of excessive NO initiated the mitochondrial apoptotic pathway. Exposure to Cd increased the mRNA and the protein expression levels of iNOS, caspase-3, Bax, p53, and Cyt-c. Furthermore, the ratio of Bax/Bcl-2 increased, while the expression of Bcl-2 decreased. Treatment with Se significantly alleviated Cd-induced apoptosis in chicken livers, as evidenced by a reduction in the production of NO, iNOS activity, the number of apoptotic cells, and mRNA and protein expression levels of iNOS, caspase-3, Bax, and Cyt-c. It indicated that Cd induced NO-mediated apoptosis through the mitochondrial apoptotic pathway and Se exerted antagonizing effects. The present study provides new insights as to how Se affects Cd-induced toxicity in the chicken liver.

show abstract

Determination of Optimal Toxic Concentration and Accumulation of Cadmium in Broiler Chicks

Cited by 9 publications

References 15 publications

Coral fossil: A potential adsorbent of natural source for cadmium removal in broilers

Coral fossil: A potential adsorbent of natural source for cadmium removal in broilers

Antagonism of cadmium-induced liver injury in ducks by α-bisabolol

The Effect of Selenium on the Cd-Induced Apoptosis via NO-Mediated Mitochondrial Apoptosis Pathway in Chicken Liver

Contact Info

Product

Resources

About