Effects of Anesthesia with Pentobarbital/Ketamine on Mitochondrial Permeability Transition Pore Opening and Ischemic Brain Damage.

Background And Objective: The alteration of mitochondrial functions, especially the opening of the mitochondrial permeability transition pore (mPTP), has been proposed as a key mechanism in the development of lesions in cerebral ischemia, wherefore it is considered as an important target for drugs against ischemic injury. In this study, we aimed to investigate the effects of mitochondrial complex I inhibitors as possible regulators of mPTP using an in vitro brain ischemia model of the pentobarbital/ketamine (PBK)-anesthetized rats.

Results: We found that PBK anesthesia itself delayed Ca-induced mPTP opening and partially recovered the respiratory functions of mitochondria, isolated from rat brain cortex and cerebellum.

Data on effects of rotenone on calcium retention capacity, respiration and activities of respiratory chain complexes I and II in isolated rat brain mitochondria.

The data presented in this article are related to the research article entitled "Rotenone decreases ischemia-induced injury by inhibiting mitochondrial permeability transition in mature brains" (Rekuviene et al., 2017) [1]. Data in this article present the direct effects of rotenone on calcium retention capacity (CRC) in isolated normal cortex and cerebellum mitochondria, effects of rotenone intravenous infusion on leak and phosphorylating respiration rates of isolated cortex and cerebellum mitochondria, on activities of respiratory chain complexes I and II in freezed-thawed/sonicated cortex and cerebellum mitochondria after brain ischemia.

Rotenone decreases ischemia-induced injury by inhibiting mitochondrial permeability transition in mature brains.

The mitochondrial permeability transition pore (mPTP) is thought to be implicated in brain ischemia-induced cell death. Here we sought to determine whether complex I (CI) of the mitochondrial electron transfer system may be involved in regulation of mPTP opening during ischemia and whether a specific inhibitor of this complex - rotenone can protect against ischemia-induced cell death in an experimental model of total ischemia in adult rat brains. Anesthetized Wistar rats were administered a single injection of rotenone (0.

The effects of cadmium chloride and sodium selenite on protein synthesis in mouse liver.

The study aimed at evaluating the effects of cadmium and selenite ions on protein synthesis and metallothioneins content in mice liver after 2 h, 8 h, 24 h and 14 days of exposure. Our studies revealed that cadmium suppressed protein synthesis after 2 h and 24 h, but activated after 8h and 14 days. Also, the endogenous mRNA translation were reduced under any exposure to cadmium, meanwhile, metallothioneins content was decreased after 2 h, but then was progressively increasing up to 492% after 14 days.

Estradiol-induced protection against ischemia-induced heart mitochondrial damage and caspase activation is mediated by protein kinase G.

We have previously reported that estradiol can protect heart mitochondria from the ischemia-induced mitochondrial permeability transition pore-related release of cytochrome c and subsequent apoptosis. In this study we investigated whether the effect of 17-beta-estradiol on ischemia-induced mitochondrial dysfunctions and apoptosis is mediated by activation of signaling protein kinases in a Langendorff-perfused rat heart model of stop-flow ischemia. We found that pre-perfusion of non-ischemic hearts with 100nM estradiol increased the resistance of subsequently isolated mitochondria to the calcium-induced opening of mitochondrial permeability transition pore and this was mediated by protein kinase G.