Hepatoprotective effect of polyphenols isolated from virgin coconut oil against sub-chronic cadmium hepatotoxicity in rats is associated with improvement in antioxidant defense system.

Cadmium (Cd) is a ubiquitous non-essential environmental and industrial toxicant that affects various organs in humans and experimental animals. Robust evidence confirms the contribution of oxidative stress to the pathogenesis of Cd-induced hepatic damage. Potent polyphenols found in virgin coconut oil (VCO) are free radical scavengers that may be beneficial against Cd hepatotoxicity. Thus, we aimed to evaluate the possible protective effect of polyphenols isolated from VCO on Cd-induced hepatotoxicity and oxidative stress in rats. Rats were pretreated with polyphenols isolated from VCO (10, 20, and 50 mg/kg, orally) 2 weeks prior to concurrent Cd administration (5 mg/kg, orally) for 5 weeks. Subsequently, liver damage, hepatic oxidative stress, and histopathological alterations were evaluated. In vitro antioxidant assays (DPPH and FRAP) were carried out on VCO polyphenols. Cadmium induced liver damage demonstrated by significant alterations in serum markers of liver damage, as well as pronounced decrease in albumin and total protein compared to control. Further, Cd remarkably depressed hepatic activity of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), and glutathione (GSH) content. Hepatic lipid peroxidation was markedly increased as highlighted by malondialdehyde (MDA) content. Sub-chronic administration of VCO polyphenols to Cd-treated rats produced a significant hepatoprotective effect and restored hepatic oxidative stress markers comparable to control. The prominent improvement in histopathology of rat liver confirmed the biochemical findings. The findings suggest potential beneficial effect of VCO polyphenols on Cd-induced hepatotoxicity and oxidative stress in rats; the mechanism underlying this action is associated with improvement in antioxidant defense system.

Altered gestational outcomes and delayed pubertal onset in prenatally and early postnatally food restricted male and female rats: mitigation by quercetin and kaempferol.

Nutrigenomic malnutrition during pregnancy and early postnatal life has serious consequences on original organ-programing, growth pattern, puberty and quality of life. The aim of this was to investigate the effect of two notable flavonoids, quercetin and kaempferol, with nutrigenomic potentials on prenatal and early postnatal food restrictions or both on gestational outcomes and the onset of puberty in male and females Wister rats. In three sets of experiments consisting of prenatal, postnatal food deprivations or both, rats were distributed into various treatment groups (n = 6). Prenatal food restriction (PrNFR) was initiated by 50% of ad libitum available diet in pregnancy (days 1-22) simultaneously with quercetin (50, 100 and 200 mg/kg, p.o./day) or kaempferol (50, 100 and 200 mg/kg, p.o./day) until delivery. However, postnatal food restriction (PsNFR) was simulated by litter-increment to 16 pups per mother from postnatal day 2 together with quercetin (50-200 mg/kg, p.o.) or kaempferol (50-200 mg/kg, p.o.) treatments until weaning (day 24) respectively. The last experiment encompasses both protocols with similar treatment protocols. Kaempferol attenuated PrNFR-induced alterations in gestational length compared to PrNFR-control. Quercetin and kaempferol significantly (P < 0.05) normalized nose-length of pups of rats exposed to PrNFR. Quercetin and kaempferol reduced the number of stillbirths due to PrNFR. Both also reduced the delay in pubertal onset as evidenced by normal onset of balanopreputial-separation and vaginal-opening in the PrNFR, PsNFR and PrNFR-PsNFR male and female rats respectively. Together, quercetin and kaempferol prevents prenatal and postnatal malnutrition-induced altered gestational outcomes and pubertal delays in rats.

Consumption of calcium carbide-ripened banana by pregnant rats may programme for infertility in female offspring.

One of the substances used in force ripening fruits is commercial grade calcium carbide (CaC2) which contains impurities such as arsine and this has been associated with low birth weight and fetal loss. There is thus a need to further investigate additional risks on offspring. This study was thus designed to evaluate the possible effects of maternal consumption of banana pulp force ripened with CaC2 on the offspring. Sixteen pregnant rats were randomly divided into two test groups and controls of four rats each. Two test groups were fed with pelletized feed mixed with banana pulp ripened by commercial grade CaC2 at concentrations of 50g/5kg and 100g/5kg while the controls had a group fed with pelletized feed mixed with normal ripened banana and another had only pelletized feed. This feeding pattern was done morning and evening ad libitum throughout the gestation period of twenty-one days after which only pelletized feed and water was administered. At delivery, all male offspring were separated and each dam was allowed eight female pups to nurse. Upon weaning after twenty-one days, the mothers were removed leaving eight female offspring in each group. Development of their reproductive system was monitored and recorded using parameters such as vaginal opening day (VOD) and reproductive hormonal assay at the sixth week. A fertility test was also carried out by introducing viable male rats for mating at sixth week postpartum. Trace amount of arsenic was found in the banana pulp of 100g/5kg CaC2 group (0.35ppb). CaC2 exposure was related to delayed onset in puberty, decreased serum FSH and a decreased fertility rate in the 100g/5kg CaC2 group (p<0.05). Consumption of contaminated CaC2 ripened fruits exposes humans to arsenic acid which has harmful effects on reproductive development of offspring.

Prenatal and early postnatal food restrictions cause changes in brain oxidative status and orexigenic/anorexigenic hormones in the offspring of rats: prevention by quercetin and kaempferol.

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 â€‹= â€‹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 â€‹mL/kg), quercetin (50, 100 and 200 â€‹mg/kg, p.o.) or kaempferol (50, 100 and 200 â€‹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 â€‹< â€‹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.

The Impact of Plasmodium Berghei Exposure In-utero on Neurobehavioral Profile in Mice.

INTRODUCTION: The World Health Organization estimates that about 25 million pregnant mothers are currently at risk for malaria, and that malaria accounts for over 10,000 maternal and 200,000 neonatal deaths per year. The current hypothesis of early life programming supports the premise that many developmental delay and disorders may have their origin In-utero. Therefore, the current study aimed at evaluating the possible impact of experimental malaria exposure In-utero on neurobehavioral profile in mice offspring. METHODS: Pregnant mice were intraperitoneally infected on gestational day 13 with 1.02×105 infected red blood cells. Pregnant mice (both infected and uninfected) were allowed to deliver and the offspring were monitored up to postnatal day 42 when anxiety-like, Obsessive-Compulsive Disorder (OCD), and locomotor activity were evaluated using elevated plus maze, marble burying, and Open Field Test, respectively. RESULTS: The current study showed that maternal infection with Plasmodium berghei resulted in an interesting behavior in offspring characterized by increased anxiety-like and OCD behaviors. Locomotor activity was however not affected. CONCLUSION: It may be concluded that In-utero exposure to experimental malaria in mice causes behavioral changes.

Potential link between Complement 5a Receptor and mood disorders in mouse exposed to experimental malaria in utero.

In Africa, a large number of pregnancies are exposed to Plasmodium falciparum infection. The in-utero environment extremely influences childhood neurodevelopment and behaviour. The complement 5a receptor (C5aR) is linked to several disease conditions. However, the influence of Plasmodium berghei during pregnancy on maternal complement 5a receptor and subsequently on fetal behaviour is unknown. Pregnant mice were intra-peritoneally inoculated on gestational day 13 with 1.02x105 infected red blood cells (iRBCs). iRBCs used in this experiment were gotten by in vivo passage of P. berghei in mice when the level of iRBCs have gotten to about 10-20%. A section of pregnant mice (both test and control groups) were earmarked to give birth and their offspring monitored up to postnatal day 42 when depression-like behaviour was evaluated using tail suspension test model. The other pregnant mice were subjected to cardiac puncture on gestational day 19 for C5a receptor estimation using Elisa assay. Results showed that pregnant mice infected with P. berghei had elevated C5a receptor compared with uninfected pregnant females. It was also shown that P. berghei-exposed offspring presented a depressive-like behaviour compared to unexposed controls. It may be concluded from this study, that complement 5a receptor demonstrates a pathogenic role in signaling and its possible role in mediating depression linked to Plasmodium berghei exposure in utero.

Predisposing factors associated with uncomplicated type 2 diabetes among adults in a diabetic clinic, Enugu State, Nigeria.

BACKGROUND: The role of micronutrients and other predisposing factors associated with the aetiology of type 2 diabetes in Nigeria is not well established. The objectives of this study were to investigate predisposing factors associated with uncomplicated type 2 diabetes among a Nigerian adult population. METHODS: Predisposing factors associated with uncomplicated type 2 diabetes were investigated in 60 Igbo (a major tribe in Eastern Nigeria) adults aged 30-90 years. This study was carried out at the Diabetic Clinic, University of Nigeria Teaching Hospital (UNTH) Ituku-Ozalla, Enugu. Packed cell volume (PCV), serum ferrtin and some anthropometric parameters were measured alongside fasting blood sugar (FBS). RESULTS: PCV recorded a statistically significant lower (p<0.001) mean value at 32.94±0.61% in the patients when compared with the control group with a mean value of 39.06±1.02%. Serum ferritin revealed a statistically significant higher (p<0.01; 110.20±15.17 ng/ml) mean value in the patients when compared with the control group (20.4±5.64 ng/ml). However, PCV (32.00±0.88%) and body mass index (BMI) (31.99±1.12 Kg/m(2)) recorded a statistically significant lower (p<0.05) mean value in female patients when compared with their corresponding males. There was no significant correlation (p>0.05) between serum iron ferritin, FBS and all other anthropometric predictors of incidence of type 2 diabetes. CONCLUSION: Type 2 diabetes is not associated with elevated levels of serum iron ferritin. Hence, serum ferritin may not be a better predictor of type 2 diabetes, especially in uncomplicated cases.

Mechanism of delayed puberty in rats whose mothers consumed Hibiscus sabdariffa during lactation.

CONTEXT: Extract of the calyx of Hibiscus sabdariffa Linn. (HS) (Malvaceae) has been reported to decrease fluid and food intake in lactating rats through a mechanism not yet fully understood. It has also been reported that rat pups undernourished during lactation have delayed puberty onset, suggesting a link between nutrition and onset of puberty. There is paucity of data addressing the effect of maternal consumption of HS during lactation on the onset of puberty in the female offspring. OBJECTIVE: The present study was designed to investigate whether consumption of HS during lactation will affect the onset of puberty and to examine the possible mechanism underlying this. MATERIALS AND METHODS: Lactating Sprague-Dawley rats were randomly grouped into three on postnatal day one. One group had tap water (control); another had 0.6 g aqueous HS extract/100 mL, while the third had 1.8 g aqueous HS extract/100 mL as their drinking solution throughout lactation. Maternal fluid consumption, food consumption, weight gain, plasma Na(+) and corticosterone concentrations were determined. Offspring weights were recorded at 0, 21, 28, 35, and 42 days. Ages at onset of puberty and body weights were also recorded. RESULTS: A decreased maternal fluid and food intake and an increased maternal plasma Na(+) and corticosterone concentration were observed in HS dams. The HS treated female offspring showed delayed onset of puberty. DISCUSSION AND CONCLUSION: The accelerated growth and delayed puberty in the HS offspring may be through increased corticosterone and decreased leptin delivery through breast milk.