Frank Watt

Publications (2)8.06 Total impact

• Article: Zinc supplementation prevents cardiomyocyte apoptosis and congenital heart defects in embryos of diabetic mice.

  Srinivasan Dinesh Kumar, Murugaiyan Vijaya, Ramar Perumal Samy, S Thameem Dheen, Minqin Ren, Frank Watt, Y James Kang, Boon-Huat Bay, Samuel Sam Wah Tay
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  ABSTRACT: Oxidative stress induced by maternal diabetes plays an important role in the development of cardiac malformations. Zinc (Zn) supplementation of animals and humans has been shown to ameliorate oxidative stress induced by diabetic cardiomyopathy. However, the role of Zn in the prevention of oxidative stress induced by diabetic cardiac embryopathy remains unknown. We analyzed the preventive role of Zn in diabetic cardiac embryopathy by both in vivo and in vitro studies. In vivo study revealed a significant decrease in lipid peroxidation, superoxide ions, and oxidized glutathione and an increase in reduced glutathione, nitric oxide, and superoxide dismutase in the developing heart at embryonic days (E) 13.5 and 15.5 in the Zn-supplemented diabetic group when compared to the diabetic group. In addition, significantly down-regulated protein and mRNA expression of metallothionein (MT) in the developing heart of embryos from diabetic group was rescued by Zn supplement. Further, the nuclear microscopy results showed that trace elements such as phosphorus, calcium, and Zn levels were significantly increased (P<0.001), whereas the iron level was significantly decreased (P<0.05) in the developing heart of embryos from the Zn-supplemented diabetic group. In vitro study showed a significant increase in cellular apoptosis and the generation of reactive oxygen species (ROS) in H9c2 (rat embryonic cardiomyoblast) cells exposed to high glucose concentrations. Supplementation with Zn significantly decreased apoptosis and reduced the levels of ROS. In summary, oxidative stress induced by maternal diabetes could play a role in the development and progression of cardiac embryopathy, and Zn supplementation could be a potential therapy for diabetic cardiac embryopathy.
  Free radical biology & medicine 07/2012; 53(8):1595-606. · 5.42 Impact Factor
• Article: Carboxylate microsphere-induced cellular toxicity in human lung fibroblasts.

  Ramar Perumal Samy, Cheng-Teng Ng, Boon-Huat Bay, Frank Watt
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  ABSTRACT: Carboxylate microspheres (CMs) are mainly used in industrial, biomedical and various household products. In this study, we assessed the cytotoxic effects of CMs on human MRC-5 lung fibroblasts by using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. Oxidative stress was determined by measurements of reactive oxygen species and antioxidant (superoxide dismutase and catalase) levels and proinflammatory cytokines quantified by enzyme-linked immunosorbent assay. Morphological changes were examined by light microscopy, confocal microscopy and transmission electron microscopy. The lung fibroblasts were exposed to increasing concentrations of CMs (0.1-1000 μmol/L) for 24 h. The results showed significant changes in cell morphology with induction of cytotoxicity and oxidative stress observed in 10-1000 μmol/L concentrations of CM-treated fibroblasts. Ultrastructural examination revealed the presence of CMs inside the cytoplasm of treated lung fibroblasts. CMs also induced elevated interleukin (IL)-1, IL-6, IL-8, IL-10 and tumor necrosis factor α levels at higher concentrations. We have demonstrated that CMs significantly reduce cell viability in a dose-dependant manner in lung fibroblasts at 0.1-1000 μmol/L doses. The findings suggest that high doses of CMs have the potential to induce cellular toxicity to the lung in vitro.
  Experimental Biology and Medicine 06/2012; 237(6):635-43. · 2.64 Impact Factor