Mitochondrial function in lungs of rats with different susceptibilities to hyperoxia-induced acute lung injury.

Adult rats exposed to hyperoxia (>95% O) die from respiratory failure in 60-72 h. However, rats preconditioned with >95% O for 48 h followed by 24 h in room air acquire tolerance of hyperoxia (H-T), whereas rats preconditioned with 60% O for 7 days become more susceptible (H-S). Our objective was to evaluate lung tissue mitochondrial bioenergetics in H-T and H-S rats.

Depolarized mitochondrial membrane potential and protection with duroquinone in isolated perfused lungs from rats exposed to hyperoxia.

Dissipation of mitochondrial membrane potential (Δψ) is a hallmark of mitochondrial dysfunction. Our objective was to use a previously developed experimental-computational approach to estimate tissue Δψ in intact lungs of rats exposed to hyperoxia and to evaluate the ability of duroquinone (DQ) to reverse any hyperoxia-induced depolarization of lung . Rats were exposed to hyperoxia (>95% O) or normoxia (room air) for 48 h, after which lungs were excised and connected to a ventilation-perfusion system.

Assessment of Protection Offered By the NRF2 Pathway Against Hyperoxia-Induced Acute Lung Injury in NRF2 Knockout Rats.

Nuclear factor erythroid 2-related factor (Nrf2) is a redox-sensitive transcription factor that responds to oxidative stress by activating expressions of key antioxidant and cytoprotective enzymes via the Nrf2-antioxidant response element (ARE) signaling pathway. Our objective was to characterize hyperoxia-induced acute lung injury (HALI) in Nrf2 knock-out (KO) rats to elucidate the role of this pathway in HALI. Adult Nrf2 wildtype (WT), and KO rats were exposed to room air (normoxia) or >95% O2 (hyperoxia) for 48 h, after which selected injury and functional endpoints were measured in vivo and ex vivo.

Tissue response to biphasic calcium phosphate ceramic with different ratios of HA/beta TCP in periodontal osseous defects.

The purpose of this study was to determine the optimal ratio of calcium hydroxyapatite (HA) to beta tricalcium phosphate (beta TCP) in a biphasic porous calcium phosphate (BCP) ceramic for effective repair of periodontal osseous defects. Defects were surgically produced in beagle dogs and made chronic for 4 months to simulate periodontal disease. Mucoperiosteal periodontal flaps were reflected, followed by osseous defect debridement and root planing.