scholarly journals Maternal obesity and overnutrition increase oxidative stress in male rat offspring reproductive system and decrease fertility

2014 ◽  
Vol 39 (4) ◽  
pp. 549-556 ◽  
Author(s):  
G L Rodríguez-González ◽  
C C Vega ◽  
L Boeck ◽  
M Vázquez ◽  
C J Bautista ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reproductive System ◽  
Maternal Obesity ◽  
Male Rat ◽  
Rat Offspring

scholarly journals Early Postweaning Treatment with Dimethyl Fumarate Prevents Prenatal Dexamethasone- and Postnatal High-Fat Diet-Induced Programmed Hypertension in Male Rat Offspring

2018 ◽  
Vol 2018 ◽  
pp. 1-8 ◽  
Author(s):  
Yu-Ju Lin ◽  
I-Chun Lin ◽  
Hong-Ren Yu ◽  
Jiunn-Ming Sheen ◽  
Li-Tung Huang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Dimethyl Fumarate ◽  
Nutrient Sensing ◽  
Male Rat ◽  
Related Factor ◽  
High Fat ◽  
Antenatal Corticosteroids ◽  
Rat Offspring ◽  
Nrf2 Signaling Pathway ◽  
The Impact

Prenatal dexamethasone (DEX) exposure, postnatal high-fat (HF) intake, and oxidative stress are closely related to the development of hypertension. Nuclear factor erythroid-derived 2-related factor 2 (Nrf2) regulates oxidative stress. Dimethyl fumarate (DMF) reportedly activates Nrf2 and protects against oxidative stress damage. We examined a 4-month-old male rat offspring from five groups (n=8 for each group): control, DEX (0.1 mg/kg i.p. from a gestational age of 16 to 22 days), HF (D12331 diet from weaning to 4 months of age), and DEX + HF, DEX + HF + DMF (50 mg/kg/day via gastric gavage for 3 weeks after weaning). We found that postnatal HF intake aggravated prenatal DEX-induced hypertension in adult male offspring, which could be prevented by DMF treatment. The beneficial effects of DMF treatment include an increase in renal Nrf2 gene expression, reduction of oxidative stress, decrease in plasma asymmetric dimethylarginine (ADMA) and renal soluble epoxide hydrolase protein levels, increase in the L-arginine-to-ADMA ratio, and activation of genes related to nutrient sensing and autophagy (e.g., Pparb, Pparg, Ppargc1a, Ulk1, and Atg5). In conclusion, better understanding of the impact of the Nrf2 signaling pathway in the two-hit model will aid in protecting children exposed to antenatal corticosteroids and a postnatal HF diet from programmed hypertension.

scholarly journals Accelerated aging of reproductive capacity in male rat offspring of protein-restricted mothers is associated with increased testicular and sperm oxidative stress

AGE ◽  
2014 ◽  
Vol 36 (6) ◽  
Author(s):  
Guadalupe L. Rodríguez-González ◽  
Luis A. Reyes-Castro ◽  
Claudia C. Vega ◽  
Lourdes Boeck ◽  
Carlos Ibáñez ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Accelerated Aging ◽  
Reproductive Capacity ◽  
Male Rat ◽  
Rat Offspring

scholarly journals MATERNAL OBESITY PROGRAMS EARLY AGING OF MALE RAT OFFSPRING (F1) LIVER METABOLISM AND TRANSCRIPTOME

2017 ◽  
Vol 1 (suppl_1) ◽  
pp. 859-859
Author(s):  
C. Lomas-Soria ◽  
C.J. Bautista ◽  
L.A. Reyes-Castro ◽  
C. Ibañez-Chavez ◽  
G.L. Rodríguez-González ◽  
...  
Keyword(s):  
Maternal Obesity ◽  
Liver Metabolism ◽  
Male Rat ◽  
Rat Offspring ◽  
Early Aging

scholarly journals Maternal Exposure to Bisphenol A Combined with High-Fat Diet-Induced Programmed Hypertension in Adult Male Rat Offspring: Effects of Resveratrol

2019 ◽  
Vol 20 (18) ◽  
pp. 4382 ◽  
Author(s):  
Chien-Ning Hsu ◽  
Yu-Ju Lin ◽  
You-Lin Tain
Keyword(s):  
Oxidative Stress ◽  
Bisphenol A ◽  
Signaling Pathway ◽  
Adult Male ◽  
Endocrine Disrupting Chemicals ◽  
Maternal Exposure ◽  
Male Rat ◽  
High Fat ◽  
Rat Offspring ◽  
No Bioavailability

Maternal exposure to endocrine disrupting chemicals (EDCs) and a high-fat intake may induce the developmental programming of hypertension in adult offspring. Bisphenol A (BPA) is one of the most commonly environmental EDCs. As the nitric oxide (NO) and aryl hydrocarbon receptor (AHR) signaling pathways both contribute to the pathogenesis of hypertension, we evaluated whether resveratrol, an antioxidant and an AHR antagonist, can prevent hypertension programmed by a maternal BPA and HF diet. Sixteen-week-old male rat offspring were assigned to six groups (n = 8 per group): Control, HF (D12331, Research Diets), BPA (50 μg/kg/day), HF + BPA, BPA + R (resveratrol 50mg/L in drinking water throughout pregnancy and lactation), and HF + BPA + R. Maternal BPA exposure exacerbated hypertension programmed by HF consumption in adult male offspring, which was protected by maternal resveratrol therapy. The BPA and HF diet synergistically induced oxidative stress in offspring kidneys, which resveratrol treatment prevented. We observed that HF + BPA-induced programmed hypertension was associated with a decreased NO bioavailability, increased oxidative stress, and an activated AHR signaling pathway. The beneficial effects of resveratrol are relevant to restoring NO bioavailability, reducing oxidative stress, and antagonizing the AHR signaling pathway. Our results cast a new light on resveratrol as a reprogramming strategy to protect against hypertension programmed by combined BPA and HF exposure, but this strategy has yet to be translated into clinical applications.

scholarly journals Protection of Male Rat Offspring against Hypertension Programmed by Prenatal Dexamethasone Administration and Postnatal High-Fat Diet with the Nrf2 Activator Dimethyl Fumarate during Pregnancy

2019 ◽  
Vol 20 (16) ◽  
pp. 3957 ◽  
Author(s):  
Chien-Ning Hsu ◽  
Yu-Ju Lin ◽  
Hong-Ren Yu ◽  
I-Chun Lin ◽  
Jiunn-Ming Sheen ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Dimethyl Fumarate ◽  
Nutrient Sensing ◽  
Male Rat ◽  
Adult Offspring ◽  
Related Factor ◽  
High Fat ◽  
Male Adult ◽  
Rat Offspring ◽  
Nrf2 Signaling Pathway

Hypertension can originate from early-life exposure to oxidative stress. As reported, dimethyl fumarate (DMF) activates nuclear factor erythroid-derived 2-related factor 2 (Nrf2) and protects against oxidative stress damage. We examined whether maternal DMF therapy protects adult offspring against hypertension programmed by prenatal dexamethasone (DEX) and postnatal high-fat (HF) diet exposure. We examined male Sprague Dawley rat offspring at 4 months of age from five groups (n = 11–13/group): control, DEX (0.1mg/kg i.p. from gestational day 16 to 22), HF (D12331 diet from weaning to 16 weeks of age), DEX+HF, and DEX+HF+DMF (50mg/kg/day via gastric gavage for 3 weeks during pregnancy). Maternal DMF therapy prevented male offspring against hypertension programmed by combined DEX and HF exposures. The protective effects of maternal DMF include reduced oxidative stress, decreased plasma asymmetric dimethylarginine (ADMA) levels, downregulated the renin-angiotensin system (i.e. Ren, Agt, Ace, and Agtr1a), increased renal protein levels of certain nutrient-sensing signals, and promoted autophagy. In conclusion, maternal Nrf2 activation by DMF protects male adult offspring against hypertension programmed by combined DEX and HF exposures. Our results cast a new light on the therapeutic potential of targeting Nrf2 signaling pathway as reprogramming strategies to prevent programmed hypertension in children exposed to antenatal corticosteroids and postnatally excessive consumption of fat.

scholarly journals Toxoplasma gondii: A Possible Inducer of Oxidative Stress in Re-productive System of Male Rats

2020 ◽  
Author(s):  
Ziba HOSEINY ASL NAZARLU ◽  
Mohammad MATINI ◽  
Maryam BAHMANZADEH ◽  
Faeze FOROUGHI-PARVAR
Keyword(s):  
Oxidative Stress ◽  
Toxoplasma Gondii ◽  
Adverse Effects ◽  
Reproductive System ◽  
Male Rats ◽  
Male Rat ◽  
Post Inoculation ◽  
Productive System ◽  
Testis Tissue

Results: After post inoculation, the variations of the OSMs in the testis tissue of infected rats were as follows: a significant decrease of SOD on day 80 (P=0.03), and CAT activity were detected on day 60 and 80 (P=0.04 and P=0.01) respectively.  In addition, GSH (P =0.01) and TAC (P =0.03) concentration were significantly reduced on day 80. On the contrary, the concentration of MDA (P =0.01) was increased 70 days after infection. In addition, consistent changes with the tissue testis were observed in the serum OSMs of infected rats. Conclusion: T. gondii infection caused oxidative stress in testis tissue. Thus, the adverse effects of oxidative stress may affect the male rat reproductive system. 

scholarly journals Maternal Resveratrol Therapy Protects Male Rat Offspring against Programmed Hypertension Induced by TCDD and Dexamethasone Exposures: Is It Relevant to Aryl Hydrocarbon Receptor?

2018 ◽  
Vol 19 (8) ◽  
pp. 2459 ◽  
Author(s):  
Chien-Ning Hsu ◽  
Yu-Ju Lin ◽  
Pei-Chen Lu ◽  
You-Lin Tain
Keyword(s):  
Oxidative Stress ◽  
Aryl Hydrocarbon Receptor ◽  
Signaling Pathway ◽  
Renin Angiotensin System ◽  
Male Rat ◽  
Beneficial Effects ◽  
Rat Offspring ◽  
Aryl Hydrocarbon ◽  
Induced Hypertension ◽  
Pregnancy And Lactation

Hypertension can originate from early-life adverse environmental in utero exposure to dexamethasone (DEX) or 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). Since DEX and TCDD are related to the aryl hydrocarbon receptor (AHR) signaling pathway, we examined whether resveratrol, an AHR modulator and antioxidant, could prevent programmed hypertension via regulating AHR signaling and oxidative stress. Groups of four-month-old male rat offspring were studied (n = 7–8 per group): control, DEX (0.1 mg/kg i.p. from a gestational age of 16 to 22 days), TCDD (200 ng/kg in four once-weekly oral doses), DEX + TCDD, and DEX + TCDD + R (resveratrol 0.05% in drinking water throughout pregnancy and lactation). Maternal TCDD exposure aggravated prenatal DEX-induced hypertension in adult male offspring, which maternal resveratrol therapy prevented. Maternal TCDD exposure aggravated DEX-induced oxidative damage in offspring kidneys, which was prevented by resveratrol therapy. Maternal resveratrol therapy decreased asymmetric and symmetric dimethylarginine (ADMA and SDMA) levels, thereby preventing combined DEX and TCDD exposure-induced programmed hypertension. Increases in renal Ahrr and Cyp1a1 expression induced by DEX + TCDD exposure were restored by resveratrol therapy. The beneficial effects of resveratrol on DEX + TCDD-induced hypertension relate to reduced renal mRNA expression of Ren, Ace, and Agtr1a expression. Thus, the beneficial effects of resveratrol on DEX + TCDD-induced hypertension include reduction of oxidative stress, restoration of nitric oxide (NO) bioavailability, blockade of the renin–angiotensin system (RAS), and antagonizing AHR signaling pathway.

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