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Brain oxidative signaling pathways have been identified as important targets for alleviating food deprivation-induced changes in metabolic gate-ways. Previous studies have shown that prenatal and early postnatal malnutrition alters leptin and ghrelin signaling via oxidative pathways. Thus, it has been hypothesized that agents with antioxidant properties might be beneficial for the mitigation of prenatal and early postnatal food scarcity-induced oxidative damage. Quercetin and kaempferol are natural bioflavonoids with proven antioxidant properties. In this study, we evaluated their effects on prenatal maternal food consumption, maternal and pup weights, biomarkers of orexigenic and anorexigenic hormones and oxidative stress in rats. Rats were allotted into different treatment groups (n ​= ​6) in three different experiments (prenatal, postnatal food-deprivations or both). Prenatal-food restriction (PrNFR) was induced by 50% of ad libitum accessible diet during pregnancy till parturition and postnatal-food restriction (PsNFR) was simulated by litter-enlargement to 16 pups per mother from postnatal day (PND) 2. Rats in each experiment were concurrently treated with vehicle (10 ​mL/kg), quercetin (50, 100 and 200 ​mg/kg, p.o.) or kaempferol (50, 100 and 200 ​mg/kg, p.o.) respectively. A third experimental group consisted of both protocols. Quercetin and kaempferol dose-dependently increased the body weights of pups exposed to PrNFR, PsNFR and PrNFR-PsNFR at PNDs 1–22 respectively. Both compounds increased maternal body weights but attenuated maternal food-intake at prenatal days 7 and 14 due by PrNFR. Quercetin and kaempferol reduced brain malondialdehyde concentrations and increased glutathione levels in PrNFR, PsNFR and PrNFR-PsNFR-exposed offspring of rats. Importantly, quercetin and kaempferol significantly ( p ​< ​0.05) prevented PrNFR-, PsNFR- or PrNFR-PsNFR-induced alterations in leptin and ghrelin levels. Cumulatively, quercetin and kaempferol increased pup and maternal weights and attenuated maternal food-intake of rats submitted to PrNFR, PsNFR and PrNFR-PsNFR respectively, likely via nutrigenomic modulations of orexigenic/anorexigenic hormones and inhibition of brain oxidative stress.

Objectives: Oxidative stress (OS)-related pathologic conditions in the tissues of living organism have been linked to exposure to stressful events within the environment. This study examined the impact of different kinds of stress exposure on glutathione (GSH)-related antioxidants. The effect of stress was examined using comparative levels of GSH, glutathione-S-transferase (GST) and glutathione peroxidase (GPx) in female Wistar rats. Materials and Methods: One hundred and sixty-eight adult female Wistar rats with body weights ranging between 150 and 200 g, were used for the study. The animals were distributed into 28 groups of six animals each. The experimental animals were routinely exposed to three different stressors; restraint chamber test, mirror chamber test and intruder chamber test for a duration of 1, 3 or 5 h per day for 1, 2 and 3 weeks, respectively. All animals were allowed free access to food (rat chaws), with water ad libitum. Animals were euthanise through cervical dislocation after the experimental period and the different target tissues were carefully harvested and homogenised for antioxidant estimation following standard procedure. Data obtained were statistically analysed and values expressed as mean ± standard error of mean and P < 0.05 level was considered as statistically significant. Results: Findings from this study elucidated the fact that exposure to stress is capable of causing marked OS and reducing GSH-based antioxidant activities in Wistar rats. A decline in the GSH level and GPx activity as observed in the study is an indication of alterations of kidney and brain tissue cellular integrity by free radicals generated during exposure to the stressors, while the observed significant increase in GST activity level in the affected tissues indicates compromised rapid exhaustion of the cellular system. Conclusion: Hence, we conclude that stress of different nature, intensity and duration can alter the levels of GSH-related antioxidants, especially in the kidney, ovary and brain tissues of stressed Wistar rats. The GSH levels in liver tissues were observed not to have changed significantly despite the oxidative damage caused by the stressors.

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