Oligomycin, an F1FO-ATPase Inhibitor, Protects Against Ischemic Acute Kidney Injury in Male but Not in Female Rats

Tanaka, Ryosuke; Takayama, Junji; Takaoka, Masanori; Sugino, Yohko; Ohkita, Mamoru; Matsumura, Yasuo

doi:10.1254/jphs.13069fp

Cited by 7 publications

(7 citation statements)

References 26 publications

(27 reference statements)

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“…Also, since mitochondria are the major producers as well as primary targets of ROS, they are thought to play a prominent role in antibiotic-induced obesity [190]. Antibiotics may either directly target ATP synthase and abrogate the ATP synthesis pathway [191], inhibit anaerobic glycolysis [192], or they may disturb the mitochondrial respiration by altering membrane ion permeability [193]. The resulting mitochondrial dysfunction may lead to defective fatty acid degradation and subsequent accumulation leading to metabolic disorders such as obesity.…”

Section: Discussionmentioning

confidence: 99%

Antibiotics-Induced Obesity: A Mitochondrial Perspective

Andrade

Jayaprakash

Bhat

et al. 2017

Public Health Genomics

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Antibiotics are the first line of treatment against infections and have contributed immensely to reduce the morbidity and mortality rates. Recently, extensive use of antibiotics has led to alterations of the gut microbiome, predisposition to various diseases and most importantly, increase in the emergence of antibiotic-resistant bacteria, which poses a major threat to global public health. Another major issue faced worldwide due to unregulated use of antibiotics in children as well as in adults is the influence of metabolism and body weight homeostasis, leading to obesity. Apart from the involvement of biosocial causes influencing diet, physical activity, and antibiotic use, pathogenesis of obesity is linked to interconnected functional alterations in cells, tissues and organs due to biochemical, epigenetic and genetic factors. Mitochondrial dysfunction is one such factor, which is becoming the primary focus of various aspects of research on multifactorial complex diseases and is providing new perspectives on etiology, biomarker-based diagnosis, and drug sensitivity. Through this review, we have made an attempt to present the interplay between use of antibiotics, obesity, and associated mitochondrial dysfunction. This may provide insights into the molecular basis, genetic predisposition and environmental triggers, which in turn may have potential clinical applications in the management of antibiotic use.

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Section: Discussionmentioning

confidence: 99%

Antibiotics-Induced Obesity: A Mitochondrial Perspective

Andrade

Jayaprakash

Bhat

et al. 2017

Public Health Genomics

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“…Based on previous reports indicating that NAD+ administered intraperitoneally at a dosage from 50 mg/kg to 200 mg/kg have beneficial cytoprotective effects, we used 100 mg/kg, which turn out to be effective in our model 17, 18 . 10 mg/kg of FK866, NAMPT inhibitor, was administrated intraperitoneally as previously described 19 ; Sirt1 siRNAs was administrated intralateroventricularlly 20 and Olig A was administrated 1 mg/ml i.p 21 .…”

Section: Methodsmentioning

confidence: 99%

Hyperbaric Oxygen Reduces Infarction Volume and Hemorrhagic Transformation Through ATP/NAD ⁺ /Sirt1 Pathway in Hyperglycemic Middle Cerebral Artery Occlusion Rats

Manaenko

Bian

et al. 2017

Stroke

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Background and purpose Energy depletion is a critical factor leading to cell death and brain dysfunction after ischemic stroke. In this study we investigated whether energy depletion is involved in hyperglycemia-induced hemorrhagic transformation (HT) after ischemic stroke and determined the pathway underlying the beneficial effects of hyperbaric oxygen (HBO). Methods After 2 hours MCAO, hyperglycemia was induced by injecting of 50% dextrose (6 ml/kg) intraperitoneally at the onset of reperfusion. Immediately after it rats were exposed to HBO at 2 atmospheres absolutes (ATA) for 1 hour. ATP synthase inhibitor Oligomycin A (Olig A), NAMPT inhibitor FK866 or Sirt1 siRNA was administrated for interventions. Infarct volume, hemorrhagic volume, neurobehavioral deficits were recorded; the level of blood glucose, ATP and NAD+ and the activity of NAMPT were monitored; the expression of Sirt1, acetylated P53, acetylated NF-κB and cleaved caspase 3 were detected by western blots; the activity of MMP-9 was assayed by zymography. Results Hyperglycemia deteriorated energy metabolism and reduced the level of ATP and NAD+, exaggerated hemorrhagic transformation, blood-brain barrier disruption and neurological deficits after MCAO. HBO treatment increased the levels of the ATP and NAD+ and consequently increased Sirt1, resulting in attenuation of hemorrhagic transformation, brain infarction as well as improvement of neurological function in hyperglycemic MCAO rats. Conclusion HBO induced activation of ATP/NAD+/Sirt1 pathway and protected blood-brain barrier in hyperglycemic MCAO rats. HBO might be promising approach for treatment of acute ischemic stroke patients, especially patients with diabetes or treated with rtPA.

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“…Diverse animal and clinical studies show renal tolerance of ischemia beyond 30 minutes, but there are concerns as to whether total recovery is possible after this period 2 . Ischemia-induced renal failure was observed one day after reperfusion was performed in male and female rats, though these renal lesions were more evident in males than in females 3 .…”

Section: Introductionmentioning

confidence: 95%

Renal biomarkers of male and female Wistar rats (Rattus norvegicus) undergoing renal ischemia and reperfusion

Bazzano¹,

Restel²,

Porfírio³

et al. 2015

Acta Cir. Bras.

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PURPOSE:To investigate biomarkers of acute renal injury in Wistar rats, subjected to left renal ischemia for 10 minutes, and then compare reperfusion at 24 hours, and at 5, 7, 14 and 21 days after the procedure. METHODS:Eight female and male rats between 60 and 81 days old were used in the Central Animal Facility of the UFMS. Assessed biomarkers included urine protein, urea, creatinine, glucose, sodium, potassium, urine alkaline phosphatase and gamma-glutamyl transferase activities, and protein-to-creatinine ratio; and in serum: urea, creatinine, sodium and potassium, fractional excretion of sodium, potassium, urine flow and creatinine clearance. RESULTS:Greater variance was observed in the parameters at 24 hours and at five days (p<0.05) after reperfusion. On the 21 st day, these parameters approximated those obtained for the control group. CONCLUSIONS:Renal ischemia for 10 minutes was sufficient to raise urine levels of protein, glucose, fractional excretion of potassium, urea, creatinine clearance, urine activity of gamma-glutamyltransferase and alkaline phosphatase enzymes in the first 24 hours, up to five days after reperfusion, which may indicate risk of acute kidney injury, according to the RIFLE classification.

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Oligomycin, an F1FO-ATPase Inhibitor, Protects Against Ischemic Acute Kidney Injury in Male but Not in Female Rats

Cited by 7 publications

References 26 publications

Antibiotics-Induced Obesity: A Mitochondrial Perspective

Antibiotics-Induced Obesity: A Mitochondrial Perspective

Hyperbaric Oxygen Reduces Infarction Volume and Hemorrhagic Transformation Through ATP/NAD ⁺ /Sirt1 Pathway in Hyperglycemic Middle Cerebral Artery Occlusion Rats

Renal biomarkers of male and female Wistar rats (Rattus norvegicus) undergoing renal ischemia and reperfusion

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Oligomycin, an F1FO-ATPase Inhibitor, Protects Against Ischemic Acute Kidney Injury in Male but Not in Female Rats

Cited by 7 publications

References 26 publications

Antibiotics-Induced Obesity: A Mitochondrial Perspective

Antibiotics-Induced Obesity: A Mitochondrial Perspective

Hyperbaric Oxygen Reduces Infarction Volume and Hemorrhagic Transformation Through ATP/NAD + /Sirt1 Pathway in Hyperglycemic Middle Cerebral Artery Occlusion Rats

Renal biomarkers of male and female Wistar rats (Rattus norvegicus) undergoing renal ischemia and reperfusion

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Hyperbaric Oxygen Reduces Infarction Volume and Hemorrhagic Transformation Through ATP/NAD ⁺ /Sirt1 Pathway in Hyperglycemic Middle Cerebral Artery Occlusion Rats