scholarly journals The role of melatonin on uteroplacental antioxidant enzymes activities and fetal growth retardation in diabetic rats (910.1)

2014 ◽  
Vol 28 (S1) ◽  
Author(s):  
Luqman Olayaki
Keyword(s):  
Antioxidant Enzymes ◽  
Fetal Growth ◽  
Growth Retardation ◽  
Diabetic Rats ◽  
Fetal Growth Retardation ◽  
Enzymes Activities ◽  
Antioxidant Enzymes Activities

scholarly journals Melatonin improves diabetes-induced foetal growth retardation in rats

2015 ◽  
Vol 18 (1) ◽  
pp. 42-47
Author(s):  
LA Olayaki ◽  
AO Soladoye ◽  
OO Ojo
Keyword(s):  
Lipid Peroxidation ◽  
Antioxidant Enzymes ◽  
Growth Retardation ◽  
Intraperitoneal Administration ◽  
Pharmaceutical Journal ◽  
Diabetic Rats ◽  
Pregnant Rats ◽  
Enzymes Activities ◽  
Foetal Growth ◽  
Antioxidant Enzymes Activities

The aim of the present study was to investigate the effect of oral melatonin administration on foetal growth retardation, utero-placental antioxidant enzymes activities and lipid peroxidation in experimental diabetic rats. Twenty pregnant rats were divided into four groups of five rats each. Diabetes mellitus was induced by a single intraperitoneal administration of 120mg/kg body weight of alloxan. From gestational day 5 to 19, 5mg/kg and 10mg/kg of oral melatonin were administered to the rats with clearly manifested gestational diabetes. On the 19th day of gestation, the rats were sacrificed by cervical dislocation and placental, foetal and uterine tissues were harvested for estimation of tissue glutathione peroxidase (GPx) activity and malondialdehyde (MDA) levels. Foetal weight, foetal size, placental and plasma glucose were also determined. Results showed that, in diabetic rats, foetal growth retardation was associated with a significant reduction in placental and uterine antioxidant enzymes (GPx) activities (P<0.001) and increased lipid peroxidation as evidenced by raised MDA concentration (P< 0.05). Treatment with oral melatonin significantly improved the foetal weight, placental and uterine antioxidant enzymes activities as well as reduced lipid peroxidation, without affecting the degree of hyperglycaemia. Effects of melatonin on foetal growth are presumed to be dependent on its ability to improve uteroplacental antioxidant enzymes activities and reduce lipid peroxidation.Bangladesh Pharmaceutical Journal 18(1): 42-47, 2015

Uteroplacental hemodynamic disturbances in establishment of fetal growth retardation in streptozocin-induced diabetic rats

Diabetes ◽  
1990 ◽  
Vol 39 (6) ◽  
pp. 743-746 ◽  
Author(s):  
N. C. Chartrel ◽  
M. T. Clabaut ◽  
F. A. Boismare ◽  
J. C. Schrub
Keyword(s):  
Fetal Growth ◽  
Growth Retardation ◽  
Diabetic Rats ◽  
Fetal Growth Retardation

The protective effect of olive cake treatment on oxidant/antioxidant biomarkers, on serum, red blood cells and liver, in streptozotocin-induced diabetic rats fed cholesterol-enriched diet

2019 ◽  
Vol 50 (4) ◽  
pp. 785-798
Author(s):  
Yahiaoui Zidan ◽  
Sherazede Bouderbala ◽  
Cherrad Hayet ◽  
Bouchenak Malika
Keyword(s):  
Lipid Peroxidation ◽  
Antioxidant Enzymes ◽  
Red Blood Cells ◽  
Blood Cells ◽  
Diabetic Rats ◽  
Male Rats ◽  
Olive Cake ◽  
Content Type ◽  
Enzymes Activities ◽  
Antioxidant Enzymes Activities

Purpose The purpose of this study is to determine the effect of olive cake (OC) on lipid peroxidation as well as antioxidant enzymes activities of serum, red blood cells (RBCs) and liver, in streptozotocin (STZ)-induced-diabetic rat fed cholesterol-enriched diet. Design/methodology/approach Hypercholesterolemic male rats were rendered diabetic (HC-D) by a single intraperitoneal injection dose of STZ (35 mg/kg BW). HC-D rats were divided into two groups fed for 28d a diet supplemented with OC at 7.5 percent (HC-D-OC) or not (HC-D). A control group (C) was submitted to standard diet containing 20 per cent casein for the same experimental period. Findings RBCs, serum and liver thiobarbituric acid reactive substances (TBARS) contents were significantly increased in HC-D, compared to C group (p = 0.04, p = 0.02 and 0.03). These values were significantly decreased (48 per cent and 64 per cent; p = 0.02 and p = 0.0007) in serum and liver of HC-D-OC vs HC-D group. In RBCs, superoxide dismutase (SOD), catalase (CAT), and glutathione S-transferase (GST) activities were, respectively, 1.5, 2- and 1.7-fold higher (p = 0.03, p = 0.008 and p = 0.03) in HC-D group compared to HC group. In serum and liver, SOD, CAT and GST activities were, respectively, 1.3-, 2.6- and 1.6-fold increased (p = 0.03, p = 0.007 and p = 0.02). In HC-D-OC compared to HC-D group, RBCs glutathione peroxidase (GSH-Px), CAT and GST activities were, respectively, 2.1-, 3.3- and 2.1-fold higher (p = 0.04, p = 0.0009 and p = 0.03). In serum, SOD and CAT activities were, respectively, 1.5- and 1.9-fold increased (p = 0.02, p = 0.02). In liver, SOD, GSH-PX, CAT and GST activities were significantly increased (p = 0.005, p = 0.03, p = 0.02 and p = 0.04). Originality/value In diabetic rats-fed cholesterol-enriched diet, OC was able to reduce oxidative stress by decreasing lipid peroxidation and increasing antioxidant enzymes activities in serum, RBCs and liver.

Fetal growth retardation syndrome and adaptation of the placenta

2016 ◽  
Vol 3 (2) ◽  
pp. 76-80 ◽  
Author(s):  
Aleksandra G. Goryunova ◽  
M. S Simonova ◽  
A. V Murashko
Keyword(s):  
Growth Factors ◽  
Fetal Growth ◽  
Growth Retardation ◽  
Placental Insufficiency ◽  
Fetal Growth Retardation

There are considered modern data on etiology, pathogenesis, course of the pregnancy, methods of diagnosing of the fetal growth retardation syndrome. There is presented information about the role of growth factors and their receptors, as well as modern views on the problem of placental insufficiency as a major cause of fetal growth retardation syndrome.

scholarly journals Leptin Distribution and Metabolism in the Pregnant Rat: Transplacental Leptin Passage Increases in Late Gestation but Is Reduced by Excess Glucocorticoids

Endocrinology ◽  
2003 ◽  
Vol 144 (7) ◽  
pp. 3024-3030 ◽  
Author(s):  
Jeremy T. Smith ◽  
Brendan J. Waddell
Keyword(s):  
Fetal Growth ◽  
Growth Retardation ◽  
Indirect Evidence ◽  
Late Pregnancy ◽  
Constant Infusion ◽  
Metabolic Clearance ◽  
Fetal Growth Retardation ◽  
Transplacental Passage ◽  
Pregnant Rat

Abstract Leptin is essential for the establishment of pregnancy and appears to promote fetal growth, but the mechanisms regulating fetal leptin exposure remain unclear. In rodents, indirect evidence suggests that fetal leptin is partly derived from the maternal circulation via transplacental passage. Indeed, the placenta expresses mRNA for Ob-Ra, one of the short forms of the leptin receptor (Ob-RS) important in leptin transport, and this expression increases markedly in late pregnancy. Therefore, we determined the transplacental passage of maternal leptin to the fetus in the rat and whether this transport increases near term in association with a rise in placental expression of Ob-RS protein. Because of the proposed role of leptin in promoting fetal growth, we also assessed the effect of glucocorticoid-induced fetal growth retardation on placental leptin transport. Anesthetized rats received a constant infusion of 125I-leptin via a jugular cannula before and at d 16 and 22 of pregnancy (term = d 23); plasma samples were obtained at 10, 20, 40, 60, 80, and 100 min, and fetuses and placentas were collected at the time of the final sample. The metabolic clearance rate of leptin fell (P &lt; 0.01) from 3.08 ± 0.23 ml/min per kg in nonpregnant rats to 2.36 ± 0.13 ml/min per kg by d 22. Transplacental passage of 125I-leptin, estimated from its concentration in the whole fetus relative to maternal plasma, increased 10-fold (P &lt; 0.005) between d 16 and d 22 of pregnancy. Over this same period, Ob-RS protein expression in the placental labyrinth zone increased by almost 2-fold. Transplacental leptin passage was reduced (P &lt; 0.05) by 77% after maternal dexamethasone treatment, whereas suppression of endogenous glucocorticoid synthesis (by metyrapone) increased (P &lt; 0.05) the transfer of maternal leptin to the fetus by 55%. These data show that transplacental passage of maternal leptin is a significant source of fetal leptin and increases markedly during late pregnancy. Consistent with the proposed role of leptin as a fetal growth factor, transplacental leptin passage is reduced in association with glucocorticoid-induced fetal growth retardation.

Fetal growth retardation in rats may result from apoptosis: Role of peroxynitrite

1996 ◽  
Vol 21 (5) ◽  
pp. 619-629 ◽  
Author(s):  
M.J.S. Miller ◽  
C.A. Voelker ◽  
S. Olister ◽  
J.H. Thompson ◽  
X-J. Zhang ◽  
...  
Keyword(s):  
Fetal Growth ◽  
Growth Retardation ◽  
Fetal Growth Retardation

Amelioration of Benzo[a]pyrene-induced oxidative stress and pulmonary toxicity by Naringenin in Wistar rats: A plausible role of COX-2 and NF-κB

2016 ◽  
Vol 36 (4) ◽  
pp. 349-364 ◽  
Author(s):  
R Ali ◽  
A Shahid ◽  
N Ali ◽  
SK Hasan ◽  
F Majed ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Antioxidant Enzymes ◽  
Pulmonary Toxicity ◽  
Radical Scavenging ◽  
Protective Agent ◽  
Enzymes Activities ◽  
Cell Counts ◽  
Antioxidant Enzymes Activities ◽  
Cox 2

Naringenin is a naturally occurring flavanones and has been found to exhibit free radical scavenging, enzyme inhibition, antioxidants, anti-inflammatory, and anticancer activities. Present study was designed to evaluate the protective role of naringenin against benzo[a]pyrene (B[a]P)-induced oxidative stress and pulmonary toxicity. Rats were treated with naringenin at a dose of 100 mg/kg body weight (b. wt.), by oral gavage. B[a]P in a single dose of 50 mg/kg b. wt. was given intraperitoneally. Total protein, total cell counts, lactate dehydrogenase, lipid peroxidation, reduced glutathione, antioxidant enzymes activities, lung histology and expression of nuclear factor kappa B (NF-κB), and cyclo-oxygenase-2 (COX-2) was assessed to evaluate protective effects of naringenin. Histopathological and immunohistochemical studies were also carried out to observe lung toxicity and inflammation. B[a]P administration enhanced the levels of lung injury markers and reduced antioxidant enzymes activities. Naringenin treatment attenuated the levels of oxidative stress by restoring antioxidant enzymes, further improved lung histological damage and significant decrease in inflammatory responses. Naringenin also effectively decreased the expression of NF-κB, and COX-2 induced by B[a]P. These findings suggest that naringenin supplementation is beneficial in maintaining the integrity of alveoli and the epithelium that may be used as a protective agent in B[a]P-induced oxidative stress and lung damage. However, further studies are warranted to elucidate the potential mechanism of action of naringenin.

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