Lactate Regulates Rat Male Germ Cell Function through Reactive Oxygen Species

The existence of hypoxia-induced reactive oxygen species (ROS) production remains controversial. However, numerous observations with a variety of methods and in many cells and tissue types are supportive of this idea. Skeletal muscle appears to behave much like heart in that in the early stages of hypoxia there is a transient elevation in ROS, whereas in chronic exposure to very severe hypoxia there is evidence of ongoing oxidative stress. Important remaining questions that are addressed in this review include the following. Are there levels of Po2 in skeletal muscle, typical of physiological or mildly pathophysiological conditions, that are low enough to induce significant ROS production? Does the ROS associated with muscle contractile activity reflect imbalances in oxygen uptake and demand that drive the cell to a more reduced state? What are the possible molecular mechanisms by which ROS may be elevated in hypoxic skeletal muscle? Is the production of ROS in hypoxia of physiological significance, both with respect to cell signaling pathways promoting cell function and with respect to damaging effects of long-term exposure? Discussion of these and other topics leads to general conclusions that hypoxia-induced ROS may be a normal physiological response to imbalance in oxygen supply and demand or environmental stress and may play a yet undefined role in normal response mechanisms to these stimuli. However, in chronic and extreme hypoxic exposure, muscles may fail to maintain a normal redox homeostasis, resulting in cell injury or dysfunction.

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Reactive oxygen species and uncoupling protein 2 in pancreatic β-cell function

Diabetes Obesity and Metabolism ◽

10.1111/j.1463-1326.2010.01269.x ◽

2010 ◽

Vol 12 ◽

pp. 141-148 ◽

Cited By ~ 61

Author(s):

J. Pi ◽

S. Collins

Keyword(s):

Reactive Oxygen Species ◽

Cell Function ◽

Uncoupling Protein ◽

Reactive Oxygen ◽

Uncoupling Protein 2 ◽

Oxygen Species ◽

Pancreatic Β Cell ◽

Β Cell ◽

Β Cell Function

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Persistent Oxidative Stress Due to Absence of Uncoupling Protein 2 Associated with Impaired Pancreatic β-Cell Function

Endocrinology ◽

10.1210/en.2008-1642 ◽

2009 ◽

Vol 150 (7) ◽

pp. 3040-3048 ◽

Cited By ~ 122

Author(s):

Jingbo Pi ◽

Yushi Bai ◽

Kiefer W. Daniel ◽

Dianxin Liu ◽

Otis Lyght ◽

...

Keyword(s):

Oxidative Stress ◽

Reactive Oxygen Species ◽

Insulin Secretion ◽

Cell Function ◽

Uncoupling Protein ◽

Mitochondrial Protein ◽

Reactive Oxygen ◽

Oxygen Species ◽

Β Cell Function ◽

Glucose Stimulated Insulin Secretion

Uncoupling protein (UCP) 2 is a widely expressed mitochondrial protein whose precise function is still unclear but has been linked to mitochondria-derived reactive oxygen species production. Thus, the chronic absence of UCP2 has the potential to promote persistent reactive oxygen species accumulation and an oxidative stress response. Here, we show that Ucp2−/− mice on three highly congenic (N >10) strain backgrounds (C57BL/6J, A/J, 129/SvImJ), including two independently generated sources of Ucp2-null animals, all exhibit increased oxidative stress. Ucp2-null animals exhibit a decreased ratio of reduced glutathione to its oxidized form in blood and tissues that normally express UCP2, including pancreatic islets. Islets from Ucp2−/− mice exhibit elevated levels of numerous antioxidant enzymes, increased nitrotyrosine and F4/80 staining, but no change in insulin content. Contrary to results in Ucp2−/− mice of mixed 129/B6 strain background, glucose-stimulated insulin secretion in Ucp2−/− islets of each congenic strain was significantly decreased. These data show that the chronic absence of UCP2 causes oxidative stress, including in islets, and is accompanied by impaired glucose-stimulated insulin secretion.

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YW1-12 Possible involvement of reactive oxygen species in heat-induced germ cell apoptosis of testis (Young Urologist Research Workshop)

The Japanese Journal of Urology ◽

10.5980/jpnjurol.95.294_4 ◽

2004 ◽

Vol 95 (2) ◽

pp. 294

Author(s):

Shingo Matsuki

Keyword(s):

Reactive Oxygen Species ◽

Germ Cell ◽

Cell Apoptosis ◽

Reactive Oxygen ◽

Oxygen Species ◽

Germ Cell Apoptosis ◽

Research Workshop

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Chronic pulsatile hyperglycemia reduces insulin secretion and increases accumulation of reactive oxygen species in fetal sheep islets

Journal of Endocrinology ◽

10.1530/joe-11-0300 ◽

2011 ◽

Vol 212 (3) ◽

pp. 327-342 ◽

Cited By ~ 11

Author(s):

Alice S Green ◽

Xiaochuan Chen ◽

Antoni R Macko ◽

Miranda J Anderson ◽

Amy C Kelly ◽

...

Keyword(s):

Reactive Oxygen Species ◽

Insulin Secretion ◽

Oxidative Damage ◽

Cell Function ◽

Reactive Oxygen ◽

Insulin Content ◽

Oxygen Species ◽

Β Cell ◽

Fetal Sheep ◽

Β Cell Function

Children from diabetic pregnancies have a greater incidence of type 2 diabetes. Our objective was to determine if exposure to mild–moderate hyperglycemia, by modeling managed diabetic pregnancies, affects fetal β-cell function. In sheep fetuses, β-cell responsiveness was examined after 2 weeks of sustained hyperglycemia with 3 pulses/day, mimicking postprandial excursions, and compared to saline-infused controls (n=10). Two pulsatile hyperglycemia (PHG) treatments were studied: mild (mPHG,n=5) with +15% sustained and +55% pulse; and moderate (PHG,n=10) with +20% sustained and +100% pulse. Fetal glucose-stimulated insulin secretion and glucose-potentiated arginine insulin secretion were lower (P<0.05) in PHG (0.86±0.13 and 2.91±0.39 ng/ml plasma insulin) but not in mPHG fetuses (1.21±0.08 and 4.25±0.56 ng/ml) compared to controls (1.58±0.25 and 4.51±0.56 ng/ml). Islet insulin content was 35% lower in PHG and 35% higher in mPHG vs controls (P<0.01). Insulin secretion and maximally stimulated insulin release were also reduced (P<0.05) in PHG islets due to lower islet insulin content. Isolated PHG islets also had 63% greater (P<0.01) reactive oxygen species (ROS) accumulation at 11.1 mmol/l glucose than controls (P<0.01), but oxidative damage was not detected in islet proteins. PHG fetuses showed evidence of oxidative damage to skeletal muscle proteins (P<0.05) but not insulin resistance. Our findings show that PHG induced dysregulation of islet ROS handling and decreased islet insulin content, but these outcomes are independent. The β-cell outcomes were dependent on the severity of hyperglycemia because mPHG fetuses had no distinguishable impairments in ROS handling or insulin secretion but greater insulin content.

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