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The three discrete [Zn 6 ] c omplexes [Na 3 Zn 6 (cpdp) 3 (μ-Bz) 3 (CH 3 OH) 6 ][ZnCl 4 ][ZnCl 3 (H 2 O)]• 3CH 3 OH•1.5H 2 O (1), [Na 3 Zn 6 (cpdp) 3 (μ-p-OBz) 3 (CH 3 OH) 6 ]• 2H 2 O (2), and [Na 3 Zn 6, have been successfully synthesized and fully characterized (Bz = benzoate; p-OBz = dianion of phydroxybenzoic acid; p-NO 2 Bz = p-nitrobenzoate). The complexes have been characterized by elemental analysis, FTIR, UV−vis, NMR spectroscopy, PXRD, and thermal analysis, including singlecrystal X-ray crystallography of 1 and 2. The molecular architectures of 1−3 are built from the self-assembly of their corresponding [Zn 2 ] units, which are interconnected to the central [Na 3 (CH 3 OH) 6 ] 3+ core by six endogenous benzoate groups, with each linking one Zn(II) and one Na(I) ion in a μ 2 :η 1 :η 1 -syn-anti bidentate fashion. The composition of the (cpdp 3− ) 3 /(Zn 2+ ) 6 complexes in 1−3 has been observed to be 1:2, on the basis of the UV−vis titration and NMR spectroscopic results, which is further supported by Xray crystallography. Systematic biological studies performed with a mice model suggested possible antidiabetic efficacy as well as anticancer activities of the complexes. When complexes 1−3 were administered intraperitoneally in mice, 1 showed a lowering in the blood glucose level, overall maintenance of the pancreatic tissue mass, restriction of DNA damage in pancreatic cells, and retention of lipid droplet (LD) frequency, whereas 2 and 3 showed hepatic tissue mass consistency by inhibiting the DNA damage in hepatic cells, prior to the exposure to a potent diabetic inducer, alloxan (ALX). Similar trends of results were observed in inhibiting the generation of reactive oxygen species (ROS) in the pancreatic and hepatic cells, as examined by spectrofluorometric methods. Thus, 1 seems to be a better compound for overall diabetic management and control, whereas 2 and 3 seem to be promising compounds for designing chemopreventive drugs against hepatic carcinoma.

Objectives: The issue of food-additive-toxicity causing several health hazards needs to be therapeutically managed in an immediate effect. Alloxan, a food additive, used for whitening and shining of flour, is capable of inducing genotoxicity, diabetes, and associated mitochondrial dysfunction. Therefore, to explore a non-toxic, phyto-based compound which could delay the onset of diabetes and prevent the multitude of damage associated therein, Chlorophyllin (CHL), was selected for our study having been reported to exhibit anti-cancer, anti-diabetes, anti-inflammatory responses. Therefore, the objectives of the present study aimed 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. Method: Mice were pre-treated with CHL through oral gavage before they were exposed to alloxan. Diabetic markers, antioxidant 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 phyto-based bioactive CHL for preventing/limiting the extent of food-additive-induced genotoxicity and mitochondrial dysfunction and serve as an advanced therapeutic tool in the management of diabetes.

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