Embryonic development and mitochondrial function. III. Inhibition of respiration and ATP generation in rat embryos by thiamphenicol

Teratology ◽  
1978 ◽  
Vol 18 (1) ◽  
pp. 93-102 ◽  
Author(s):  
Rolf Bass ◽  
Detlef Oerter ◽  
Ralf Krowke ◽  
Horst Spielmann
Keyword(s):  
Embryonic Development ◽  
Mitochondrial Function ◽  
Rat Embryos ◽  
Atp Generation

In vitro analysis of glucose metabolism and embryonic growth in postimplantation rat embryos

Development ◽  
1987 ◽  
Vol 100 (3) ◽  
pp. 431-439 ◽  
Author(s):  
S.K. Ellington
Keyword(s):  
Glucose Metabolism ◽  
Embryonic Development ◽  
Glucose Uptake ◽  
Glucose Concentration ◽  
Culture Media ◽  
Rat Embryos ◽  
Embryonic Growth ◽  
Stage Of Development

The glucose metabolism and embryonic development of rat embryos during organogenesis was studied using embryo culture. Glucose uptake and embryonic growth and differentiation of 10.5-day explants (embryos + membranes) were limited by the decreasing glucose concentration, but not the increasing concentration of metabolites, in the culture media during the second 24 h of a 48 h culture. No such limitations were found on the embryonic development of 9.5-day explants during a 48 h culture although glucose uptake was slightly reduced at very low concentrations of glucose. From the head-fold stage to the 25-somite stage of development, glucose uptake was characteristic of the stage of development of the embryo and not the time it had been in culture. Embryonic growth of 9.5-day explants was similar to that previously observed in vivo. Glucose uptake by 9.5-day explants was dependent on the surface area of the yolk sac and was independent of the glucose concentration in the culture media (within the range of 9.4 to 2.5 mM). The proportion of glucose converted to lactate was 100% during the first 42h of culture then fell to about 50% during the final 6h. The protein contents of both the extraembryonic membranes and the embryo were dependent on the glucose uptake.

scholarly journals Butylparaben Is Toxic to Porcine Oocyte Maturation and Subsequent Embryonic Development Following In Vitro Fertilization

2020 ◽  
Vol 21 (10) ◽  
pp. 3692 ◽  
Author(s):  
Pil-Soo Jeong ◽  
Sanghoon Lee ◽  
Soo-Hyun Park ◽  
Min Ju Kim ◽  
Hyo-Gu Kang ◽  
...  
Keyword(s):  
Embryonic Development ◽  
Oocyte Maturation ◽  
Mitochondrial Function ◽  
Cumulus Cell ◽  
Annexin V ◽  
Ros Generation ◽  
Vitro Fertilization ◽  
Porcine Oocyte ◽  
Mitochondrial Distribution

Parabens are widely used in personal care products due to their antimicrobial effects. Although the toxicity of parabens has been reported, little information is available on the toxicity of butylparaben (BP) on oocyte maturation. Therefore, we investigated the effects of various concentrations of BP (0 μM, 100 μM, 200 μM, 300 μM, 400 μM, and 500 μM) on the in vitro maturation of porcine oocytes. BP supplementation at a concentration greater than 300 μM significantly reduced the proportion of complete cumulus cell expansion and metaphase II oocytes compared to the control. The 300 μM BP significantly decreased fertilization, cleavage, and blastocyst formation rates with lower total cell numbers and a higher rate of apoptosis in blastocysts compared to the control. The BP-treated oocytes showed significantly higher reactive oxygen species (ROS) levels, and lower glutathione (GSH) levels than the control. BP significantly increased the aberrant mitochondrial distribution and decreased mitochondrial function compared to the control. BP-treated oocytes exhibited significantly higher percentage of γ-H2AX, annexin V-positive oocytes and expression of LC3 than the control. In conclusion, we demonstrated that BP impaired oocyte maturation and subsequent embryonic development, by inducing ROS generation and reducing GSH levels. Furthermore, BP disrupted mitochondrial function and triggered DNA damage, early apoptosis, and autophagy in oocytes.

Embryonic development and mitochondrial function

1975 ◽  
Vol 290 (2-3) ◽  
pp. 175-189 ◽  
Author(s):  
Detlef Oerter ◽  
Rolf Bass
Keyword(s):  
Embryonic Development ◽  
Mitochondrial Function

scholarly journals Inhibition of Mitochondrial Complex III in Candida Albicans ADH1 Deletion Mutant Attenuates Its Pathogenicity Significantly

2021 ◽  
Author(s):  
Hui Guo ◽  
Yi Shan Zhang ◽  
Yan Jun Song ◽  
Ya Jing Zhao ◽  
Shui Xiu Li ◽  
...  
Keyword(s):  
Mitochondrial Function ◽  
Alternative Oxidase ◽  
Oxidase Inhibitor ◽  
Complex Iii ◽  
Ros Production ◽  
Mitochondrial Complex ◽  
Aerobic Growth ◽  
Transport Chain ◽  
Atp Generation

Abstract Fermentation and aerobic respiration in mitochondria are coordinately regulated and compensated either when C. albicans grows in vitro or in the hosts, and the creature gain the strong viability. It’s insufficient to influent the growth, reproduction and pathogenicity of C. albicans by inhibiting the electron transport chain (ECT) CI, CII, CIII, CV, or fermentation related gene ADH1. Our study showed that the induction of AA (inhibitor of complex III) rather than SHAM (alternative oxidase inhibitor) abolishes the mitochondrial function completely （96% less ATP generation, 59% reduction in MMP), and increases ROS production significantly in ADH1-deleted mutant ( adh1Δ/ adh1Δ ) that in turn becomes hypersensitive to azole and apoptosis, less viable and more difficult to form hyphae. At the same time, the expression of virulence related genes ALS3 and HWP1 were significantly lower than that of WT under AA induction. Under the induction of AA, the mitochondrial function of WT was slightly damaged and cell apoptosis increased slightly，ROS production and sensitivity of azoles increased significantly, but mycelium formation and the growth of cells were not affected. Under aerobic growth, we observed an ADH1 - dependent mitochondrial effect in C. albicans demonstrated by 64% less ATP generation, 58% reduction in MMP and significant elevations of the ROS and apoptosis in ADH1 -deleted mutant. However, mycelium formation and azole susceptibility are not affected. Our results suggested that ADH1 plus CIII played an important role in antifungal activity by damaging mitochondrial function, inhibiting cell growth and hyphae formation, promoting apoptosis and reducing pathogenicity.

scholarly journals Msp1/ATAD1 restores mitochondrial function in Zellweger Spectrum Disease

2020 ◽  
Author(s):  
Esther Nuebel ◽  
Jeffrey T Morgan ◽  
Sarah Fogarty ◽  
Jacob M Winter ◽  
Sandra Lettlova ◽  
...  
Keyword(s):  
Quality Control ◽  
Mitochondrial Function ◽  
Protein Import ◽  
Model Systems ◽  
Translational Efficiency ◽  
Aaa Atpase ◽  
Peroxisomal Biogenesis ◽  
Inherited Metabolic Disorders ◽  
Atp Generation ◽  
Peroxisomal Biogenesis Disorders

Peroxisomal Biogenesis Disorders (PBDs) are a class of inherited metabolic disorders with profound neurological and other phenotypes. The most severe PBDs are caused by mutations in peroxin genes, which result in nonfunctional peroxisomes typically through impaired protein import. In order to better understand the molecular causes of Zellweger Spectrum Disease (ZSD) - the most severe PBDs -, we investigated the fate of peroxisomal mRNAs and proteins in ZSD model systems. We found that loss of peroxisomal import has no effect on peroxin mRNA expression or translational efficiency. Instead, peroxin proteins -still produced at high levels- aberrantly accumulate on the mitochondrial membrane, impairing respiration and ATP generation. Finally, we rescued mitochondrial function in fibroblasts derived from human patients with ZSD by overexpressing ATAD1, an AAA-ATPase that functions in mitochondrial quality control. These findings might provide a new focus of PBD therapies in supporting quality control pathways that protect mitochondrial function.

An investigation of non-depolarizing muscle relaxants on embryonic development in cultured rat embryos

2004 ◽  
Vol 21 (9) ◽  
pp. 715-724 ◽  
Author(s):  
A. K. Karabulut ◽  
R. Reisli ◽  
I. I. Uysal ◽  
J. B. Çelik ◽  
T. Ziylan
Keyword(s):  
Embryonic Development ◽  
Muscle Relaxants ◽  
Rat Embryos

Diminished PGE2 content, enhanced PGE2 release and defects in 3H-PGE2 transport in embryos from overtly diabetic rats

2000 ◽  
Vol 12 (4) ◽  
pp. 141 ◽  
Author(s):  
Alicia Jawerbaum ◽  
Elida T. Gonzalez ◽  
Débora Sinner ◽  
Carolina Pustovrh ◽  
Verónica White ◽  
...  
Keyword(s):  
Embryonic Development ◽  
Diabetic Rats ◽  
Rat Embryos ◽  
Pge2 Release ◽  
Uptake And Release

Diminished PGE2 levels in diabetic embryos are related to the development of malformations, and thus the aim of the present study was to determine whether PGE2 levels are modified in rat embryos cultured in diabetic serum during organogenesis, and if PGE2 content and release, and 3H-PGE2 uptake and release, are altered in incubated diabetic embryos. Rats were made diabetic by steptozotocin (60 mg kg–1) before mating. Control rat embryos cultured for 24 h (explantation Day 9) in the presence of diabetic serum showed diminished PGE2 levels. When Day 10 diabetic embryos were incubated, embryo PGE2 levels were lower, but the PGE2 released to the incubation media was much higher than in controls. Uptake of 3H-PGE2 by diabetic embryos was initially enhanced (5–10 min), then reached similar levels to controls (20–100 min). Release of 3H-PGE2 previously incorporated during a 60-min incubation was greater in diabetic embryos than in controls. These results show diminished PGE2 content in both diabetic and normal embryos cultured in the presence of diabetic serum, but suggest that diabetic embryos have the capability to produce and release high levels of PGE2. The enhanced release of PGE2 is probably the result of transport abnormalities, and leads to the elevated PGE2 concentrations found in the incubating medium and to the diminished intraembryonic PGE2 levels that alter embryonic development.

An investigation of non-depolarizing muscle relaxants on embryonic development in cultured rat embryos

2004 ◽  
Vol 21 (9) ◽  
pp. 715-724
Author(s):  
A. K. Karabulut ◽  
R. Reisli ◽  
I. I. Uysal ◽  
J. B. Çelik ◽  
T. Ziylan
Keyword(s):  
Embryonic Development ◽  
Muscle Relaxants ◽  
Rat Embryos

scholarly journals Fe(III) Is Essential for Porcine Embryonic Development via Mitochondrial Function Maintenance

PLoS ONE ◽  
2015 ◽  
Vol 10 (7) ◽  
pp. e0130791 ◽  
Author(s):  
Ming-Hui Zhao ◽  
Shuang Liang ◽  
Seon-Hyang Kim ◽  
Xiang-Shun Cui ◽  
Nam-Hyung Kim
Keyword(s):  
Embryonic Development ◽  
Mitochondrial Function
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