Alleviation of Cadmium Chloride-Induced Acute Genotoxicity, Mitochondrial DNA Disruption, and ROS Generation by Chocolate Coadministration in Mice Liver and Kidney Tissues.
Hanan Ramadan Hamad MohamedPublished in: Biological trace element research (2021)
Increased human exposure to cadmium compounds through ingesting contaminated food, water, and medications causes negative long-term health effects, which has led to the focus of recent researches on finding natural antioxidants to mitigate cadmium-induced toxicity. Therefore, the current study was undertaken to estimate the possible ameliorative effect of chocolate coadministration on acute cadmium chloride (CdCl2)-induced genomic instability and mitochondrial DNA damage in mice liver and kidney tissues. Concurrent administration of chocolate with CdCl2 dramatically decreased the DNA damage level and the number of apoptotic and necrotic cells compared to mice given CdCl2 alone. Extra-production of reactive oxygen species and increased expression of inducible nitric oxide synthase and heat shock proteins genes caused by CdCl2 administration were also highly decreased after chocolate coadministration. Conversely, chocolate coadministration restored the integrity of the mitochondrial membrane potential disrupted by CdCl2 administration, as well as the mitochondrial DNA copy number and expression level of heme oxygenase-1 gene were significantly upregulated after chocolate coadministration with CdCl2. Thus, it was concluded that the coadministration of chocolate alleviated CdCl2-induced genomic instability and mitochondrial DNA damage through its antioxidative and free radical scavenging capabilities, making chocolate a promising ameliorative product and recommended for inclusion in the daily human diet.
Keyphrases
- copy number
- mitochondrial dna
- dna damage
- oxidative stress
- diabetic rats
- genome wide
- high glucose
- endothelial cells
- heat shock
- dna methylation
- heavy metals
- reactive oxygen species
- dna repair
- induced apoptosis
- poor prognosis
- nitric oxide synthase
- drug induced
- gene expression
- cell death
- high fat diet induced
- physical activity
- long non coding rna
- squamous cell carcinoma
- induced pluripotent stem cells
- adipose tissue
- anti inflammatory
- insulin resistance
- acute respiratory distress syndrome
- human health
- heat stress
- pluripotent stem cells
- type diabetes
- climate change
- extracorporeal membrane oxygenation
- heat shock protein
- transcription factor
- rectal cancer
- signaling pathway
- drinking water
- cell cycle arrest