Title:Phyto-chlorophyllin Prevents Food Additive Induced Genotoxicity and Mitochondrial Dysfunction via Cytochrome c Mediated Pathway in Mice Model
Volume: 24
Issue: 10
Author(s): Asmita Samadder*, Sudatta Dey, Priyanka Sow, Ruchira Das, Sisir Nandi, Jayeeta Das*, Banani Bhattacharjee, Arnob Chakrovorty, Maharaj Biswas and Pradeepta Guptaroy
Affiliation:
- Department of Zoology, Cytogenetics and Molecular Biology Laboratory, University of Kalyani, Kalyani, Nadia- 741235,India
- Department of Zoology, Cytogenetics and Molecular Biology Laboratory, University of Kalyani, Kalyani, Nadia- 741235,India
Keywords:
Food additive, chlorophyllin, diabetes, mitochondria, cytochrome C, mice.
Abstract:
Objectives: The issue of food-additive-toxicity causing several health hazards needs to
be therapeutically managed with an immediate effect. Alloxan, a food additive, is used for
whitening and shining flour. It is capable of inducing genotoxicity, diabetes, and associated
mitochondrial dysfunction. Therefore, to explore a non-toxic, phyto-based compound that can
delay the onset of diabetes and prevent the multitude of damage associated, Chlorophyllin (CHL)
was selected for our study, having been reported to exhibit anti-cancer, anti-diabetes, and antiinflammatory
responses. Therefore, the objective of the present study is to evaluate the protective
role of CHL in controlling genotoxicity, glucose imbalance, and associated cytochrome c mediated
mitochondrial signaling dysfunction against food-additive-induced genotoxicity, diabetic state, and
its complexities in mice model in vivo.
Methods: Mice were pre-treated with CHL through oral gavage before they were exposed to
alloxan. Diabetic markers, anti-oxidant enzyme profile, chromosomal study, mitochondrial
functioning factors, and expression of proteins were checked against food-additive injected
mice.
Results: The results revealed that CHL pre-treatment could delay the onset of diabetes,
restrict alloxan-induced elevation of blood glucose, reduce DNA-damage and chromosomal
aberration, optimize enzymatic profile (glucokinase, pyruvate, insulin), and modulates protein
expression (insulin, IRS1, IRS2, GLUT2). Further, CHL-pre-treatment could stabilize
mitochondrial-membrane-potential, intracellular calcium ion, ATP/ADP ratio, ATPase
activity, thereby maintaining optimum functioning of cytochrome-c, bcl2, and caspase3
mitochondrial protein.
Conclusion: Therefore, the present study reports, for the first time, the screening of phytobased
bioactive CHL for preventing/limiting the extent of food-additive-induced genotoxicity
and mitochondrial dysfunction and serves as an advanced therapeutic tool in the management
of diabetes.
