Susceptibility of Glutathione-S-Transferase Polymorphism to CVD Develo- pment in Type 2 Diabetes Mellitus - A Review.

Metabolic disorder affects normal homeostasis and can lead to the development of diseases. Diabetes mellitus is the most common metabolic disorder, and a cluster of metabolic conditions can lead to cardiovascular disease (CVD) development. Diabetes mellitus and CVD are closely related, with oxidative stress, playing a major role in the pathophysiology. Glutathione-S-Transferases (GST) potentially play an important role by reducing oxidative stress and is found to be the underlying pathophysiology in the development of diabetes, cardiovascular diseases (CVD), etc Background: In this review, the role of GST genetic variant in the development of diabetes mellitus, CVD and diabetic vascular complications has been focused. Objectives: Based on the literature, it is evident that the GST can act as an important biochemical tool providing significant evidence regarding oxidative stress predominant in the development of diseases. Analysis of GST gene status, particularly detection of GSTM1 and GSTT1 null mutations and GSTP1 polymorphism, have clinical importance. Results: The analysis of GST polymorphism may help identify the people at risk and provide proper medical management. Genotyping of GST gene would be a helpful biomarker for early diagnosis of CVD development in DM and also in CVD cases. More studies focusing on the association of GST polymorphism with CVD development in diabetic patients will help us determine the pathophysiology better.

Data supporting the anticancer activity of posterior salivary gland (PSG) toxin from the cuttlefish Sepia pharaonis Ehrenberg (1831).

The data presented illustrated the in vitro anti-proliferative effect of the PSG toxin from the cuttlefish, Sepia pharaonis. The cytostatic potentials of the PSG toxin were determined by the lymphocyte migration inhibition assay. The PSG toxin (50 µg/ml) exhibited commendable inhibition of the migration of lymphocytes across the agarose gel matrix under the presence of lipopolysaccharide mitogen, with a mean migration index of 0.625. The cytotoxicity of the PSG toxin against selected cancer cell lines was determined using the MTT assay. The PSG toxin exhibited dose-dependent cytotoxicity against the MCF-7 breast cancer cells followed by KB (oral), HeLa (cervical) and A549 (lung) cancer cell lines. The PSG toxin also exhibited proportional release of LDH leakage by mitochondrial damage with an IC50 of 13.85 µM against MCF-7 breast cancer cells. The in vitro anticancer activity of the PSG toxin against the selected cell lines was evaluated by Karthik et al. (2017) [1].

Do prostaglandins modulate renal haemodynamic effects of endothelin-1 in conscious lambs?

To test the hypothesis that vasodilatory prostaglandins buffer the renal vasoconstrictor effects of endothelin-1 (ET-1) early in life, renal haemodynamic responses to ET-1 were measured in 2 groups of conscious, chronically instrumented lambs at 1-2 weeks of age (group I, n = 11) and 6 weeks of age (group II, n = 10). Lambs were pretreated with vehicle or 1 mg x kg(-1) indomethacin, a nonselective cyclooxygenase inhibitor, and renal haemodynamic effects were measured continuously for 1 min before (control) and 5 min after intra-arterial injection of 250 ng x kg(-1) ET-1. In group II lambs, there was a marked decrease in renal blood flow (RBF) and renal vascular conductance (RVC) elicited by ET-1 administration, as we have previously described. This response was not altered by vehicle or indomethacin pretreatment. In group I lambs, there was an initial increase but no decrease in RBF and RVC elicited by ET-1 administration, as we have previously described, and this response was also not altered by either vehicle or indomethacin. These results suggest that endogenously produced prostaglandins do not appear to modulate the renal haemodynamic effects of ET-1 in conscious lambs during postnatal maturation.