PMID- 37429534
OWN - NLM
STAT- MEDLINE
DCOM- 20230807
LR  - 20231003
IS  - 1096-0384 (Electronic)
IS  - 0003-9861 (Print)
IS  - 0003-9861 (Linking)
VI  - 744
DP  - 2023 Aug
TI  - Effects of ROS pathway inhibitors and NADH and FADH(2) linked substrates on 
      mitochondrial bioenergetics and ROS emission in the heart and kidney cortex and 
      outer medulla.
PG  - 109690
LID - S0003-9861(23)00189-3 [pii]
LID - 10.1016/j.abb.2023.109690 [doi]
AB  - Mitochondria are major sources of reactive oxygen species (ROS), which play 
      important roles in both physiological and pathological processes. However, the 
      specific contributions of different ROS production and scavenging components in 
      the mitochondria of metabolically active tissues such as heart and kidney cortex 
      and outer medulla (OM) are not well understood. Therefore, the goal of this study 
      was to determine contributions of different ROS production and scavenging 
      components and provide detailed comparisons of mitochondrial respiration, 
      bioenergetics, ROS emission between the heart and kidney cortex and OM using 
      tissues obtained from the same Sprague-Dawley rat under identical conditions and 
      perturbations. Specifically, data were obtained using both NADH-linked substrate 
      pyruvate + malate and FADH(2)-linked substrate succinate followed by additions of 
      inhibitors of different components of the electron transport chain (ETC) and 
      oxidative phosphorylation (OxPhos) and other ROS production and scavenging 
      systems. Currently, there is limited data available for the mitochondria of 
      kidney cortex and OM, the two major energy-consuming tissues in the body only 
      next to the heart, and scarce quantitative information on the interplay between 
      mitochondrial ROS production and scavenging systems in the three tissues. The 
      findings from this study demonstrate significant differences in mitochondrial 
      respiratory and bioenergetic functions and ROS emission among the three tissues. 
      The results quantify the rates of ROS production from different complexes of the 
      ETC, identify the complexes responsible for variations in mitochondrial membrane 
      depolarization and regulations of ROS production, and quantify the contributions 
      of ROS scavenging enzymes towards overall mitochondrial ROS emission. These 
      findings advance our fundamental knowledge of tissue-specific and 
      substrate-dependent mitochondrial respiratory and bioenergetic functions and ROS 
      emission. This is important given the critical role that excess ROS production, 
      oxidative stress, and mitochondrial dysfunction in the heart and kidney cortex 
      and OM play in the pathogenesis of cardiovascular and renal diseases, including 
      salt-sensitive hypertension.
CI  - Copyright (c) 2023 Elsevier Inc. All rights reserved.
FAU - Sadri, Shima
AU  - Sadri S
AD  - Department of Biomedical Engineering, Medical College of Wisconsin, Milwaukee, 
      WI, 53226, USA.
FAU - Tomar, Namrata
AU  - Tomar N
AD  - Department of Biomedical Engineering, Medical College of Wisconsin, Milwaukee, 
      WI, 53226, USA.
FAU - Yang, Chun
AU  - Yang C
AD  - Department of Physiology, Medical College of Wisconsin, Milwaukee, WI, 53226, 
      USA.
FAU - Audi, Said H
AU  - Audi SH
AD  - Department of Biomedical Engineering, Medical College of Wisconsin, Milwaukee, 
      WI, 53226, USA; Department of Biomedical Engineering, Marquette University, 
      Milwaukee, WI, 53223, USA.
FAU - Cowley, Allen W Jr
AU  - Cowley AW Jr
AD  - Department of Physiology, Medical College of Wisconsin, Milwaukee, WI, 53226, 
      USA; Cardiovascular Research Center, Medical College of Wisconsin, Milwaukee, WI, 
      53226, USA.
FAU - Dash, Ranjan K
AU  - Dash RK
AD  - Department of Biomedical Engineering, Medical College of Wisconsin, Milwaukee, 
      WI, 53226, USA; Department of Physiology, Medical College of Wisconsin, 
      Milwaukee, WI, 53226, USA; Cardiovascular Research Center, Medical College of 
      Wisconsin, Milwaukee, WI, 53226, USA; Department of Biomedical Engineering, 
      Marquette University, Milwaukee, WI, 53223, USA. Electronic address: 
      rdash@mcw.edu.
LA  - eng
GR  - R01 HL151587/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, U.S. Gov't, Non-P.H.S.
DEP - 20230708
PL  - United States
TA  - Arch Biochem Biophys
JT  - Archives of biochemistry and biophysics
JID - 0372430
RN  - 0 (Reactive Oxygen Species)
RN  - 0U46U6E8UK (NAD)
SB  - IM
MH  - Rats
MH  - Animals
MH  - Reactive Oxygen Species/metabolism
MH  - *NAD/metabolism
MH  - Rats, Sprague-Dawley
MH  - *Mitochondria/metabolism
MH  - Energy Metabolism
MH  - Kidney Cortex/metabolism
PMC - PMC10528392
MID - NIHMS1919226
OTO - NOTNLM
OT  - Forward and reverse electron transfer
OT  - Mitochondrial metabolism
OT  - NADPH oxidase
OT  - Oxidative stress
OT  - ROS emission
OT  - ROS production and scavenging
OT  - Respiration and bioenergetics
COIS- Declaration of competing interest The authors declare that they have no known 
      competing financial interests or personal relationships that could have appeared 
      to influence the work reported in this paper.
EDAT- 2023/07/11 01:07
MHDA- 2023/08/07 06:42
PMCR- 2024/08/01
CRDT- 2023/07/10 19:25
PHST- 2023/06/28 00:00 [received]
PHST- 2023/07/06 00:00 [accepted]
PHST- 2024/08/01 00:00 [pmc-release]
PHST- 2023/08/07 06:42 [medline]
PHST- 2023/07/11 01:07 [pubmed]
PHST- 2023/07/10 19:25 [entrez]
AID - S0003-9861(23)00189-3 [pii]
AID - 10.1016/j.abb.2023.109690 [doi]
PST - ppublish
SO  - Arch Biochem Biophys. 2023 Aug;744:109690. doi: 10.1016/j.abb.2023.109690. Epub 
      2023 Jul 8.