Context and objective Many studies have shown that cellular redox potential is largely determined by glutathione (GSH), which accounts for more than 90% of cellular non-protein thiols. The aim of this study was to delineate the effect of three flavonoids- namely quercetin, kaempferol and genistein and exogenous GSH on oxidative damage by the Fenton’s pathway through the GSH and GSH-redox cycle enzymes in 3T3-L1 cells. Materials and methods 3T3-L1 preadipocytes were exposed to each flavonoid and GSH at concentrations of 0, 5, 10, 15, 20 and 25 µM and then GSH levels and activities of glutathione peroxidase (GSH-Px), glutathione reductase (GSH-Rx) and superoxide dismutase (SOD) were measured. Results Exogenous GSH did not have significant effect on intracellular GSH although slight decrease was observed at 15–25 µM doses. However, each of the three flavonoids sustained intracellular GSH levels in the cells as compared to the respective controls. Quercetin had the most profound effect, followed by kaempferol and genistein in that order. GSH-Px, GSH-Rx and SOD activities increased for all the doses tested compared to their respective controls. Again, quercetin had the maximum increase in enzyme activities followed by kaempferol and genistein for the enzymes tested. Discussion and conclusion These findings suggest that the flavonoids play an important role in diminishing oxidation-induced biochemical damages. The enhancement of these enzymes may increase the resistance of the organism against oxidative damage by the Fenton’s pathway.

Objective: Oxidative stress, a common feature in cardiovascular and renal disease is associated with the causes and consequences of fetal growth restriction. Hence, renal redox status is likely an early determinant of morbidity in small-for-gestational-age (SGA) infants. In this study, we examined renal oxidative stress in naturally-farrowed SGA newborn pigs. Methods: We studied SGA newborn pigs with 52% less body weight and 59% higher brain/liver weight ratio compared with their appropriate-for-gestational-age (AGA) counterparts. Results: The kidneys of the SGA newborn pigs weighed 56% less than the AGA group. The glomerular cross-sectional area was also smaller in the SGA group. SGA newborn pigs exhibited increased renal lipid peroxidation, reduced kidney and urine total antioxidant capacity, and increased renal nitrotyrosine immunostaining. Whereas the protein expression level of NADPH oxidase (NOX)2 was unchanged, NOX4 expression was significantly higher in SGA kidneys. The level of serum potassium was lower, but serum sodium and creatinine were similar in SGA compared with AGA newborn pigs. The serum concentrations of C‐reactive protein and NGAL, the biomarkers of inflammation and early acute kidney injury were significantly elevated in the SGA group. Conclusion: Early induction of oxidative stress may contribute to the onset of kidney injury in growth-restricted infants.