PMID- 31751655
OWN - NLM
STAT- MEDLINE
DCOM- 20210223
LR  - 20210223
IS  - 1872-8278 (Electronic)
IS  - 1567-7249 (Linking)
VI  - 50
DP  - 2020 Jan
TI  - Hydrogen sulfide attenuates hyperhomocysteinemia-induced mitochondrial 
      dysfunctions in brain.
PG  - 158-169
LID - S1567-7249(19)30071-6 [pii]
LID - 10.1016/j.mito.2019.11.004 [doi]
AB  - Hyperhomocysteinemia (HHcy) has been implicated in the development of 
      neurodegenerative conditions and mild cognitive disorders. Mitochondrial 
      dysfunctions are the major mechanisms involved in homocysteine (Hcy)-induced 
      neurotoxicity. Although, hydrogen sulfide has been reported as potent 
      antioxidant, its effects on Hcy-induced mitochondrial dysfunctions have not been 
      studied. Therefore, the present study has been designed to evaluate the 
      protective effect of NaHS on Hcy-induced mitochondrial dysfunctions in brain. 
      NaHS supplementation decreased reactive oxygen species and nitrite levels in the 
      cortex and hippocampus of animals with HHcy. NaHS supplementation increased the 
      activity of mitochondrial electron transport chain components; NADH 
      dehydrogenase, cytochrome c oxidase and F0-F1 ATPase in the cortex and 
      hippocampus of HHcy animals along with in-gel activity of complex I - complex V 
      in the mitochondria isolated from the cortex and hippocampus of HHcy animals. 
      Moreover, NaHS supplementation also increased the mitochondrial complex I, II and 
      IV mediated oxygen consumption rate in Hcy treated mitochondria. NaHS 
      administration prevented the Hcy-induced mitochondrial damage as suggested by the 
      decreased mitochondrial swelling in the cortex and hippocampus of HHcy animals. 
      NaHS supplementation decreased the activity of lactate dehydrogenase isozymes 
      (1-5) in the brain regions of HHcy animals. The expression of protein kinase c delta 
      was also decreased in the brain regions of HHcy animals following NaHS 
      supplementation. This was accompanied by reduced activity of caspase-3 indicating 
      anti-apoptotic effect of H(2)S. Taken together, the findings suggest that H(2)S 
      supplementation ameliorates Hcy-induced oxidative stress and mitochondrial 
      dysfunctions suggesting H(2)S releasing drugs may be a novel therapeutic approach 
      to treat HHcy associated neurological disorders.
CI  - Copyright (c) 2019 Elsevier B.V. and Mitochondria Research Society. All rights 
      reserved.
FAU - Kumar, Mohit
AU  - Kumar M
AD  - Department of Biochemistry, Basic Medical Science Block-II, Panjab University, 
      Chandigarh 160014, India.
FAU - Sandhir, Rajat
AU  - Sandhir R
AD  - Department of Biochemistry, Basic Medical Science Block-II, Panjab University, 
      Chandigarh 160014, India. Electronic address: sandhir@pu.ac.in.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20191118
PL  - Netherlands
TA  - Mitochondrion
JT  - Mitochondrion
JID - 100968751
RN  - 0 (Biomarkers)
RN  - 0 (Nitrites)
RN  - EC 1.15.1.1 (Superoxide Dismutase)
RN  - GAN16C9B8O (Glutathione)
RN  - YY9FVM7NSN (Hydrogen Sulfide)
SB  - IM
MH  - Animals
MH  - Apoptosis/drug effects/physiology
MH  - Biomarkers
MH  - Electron Transport/drug effects
MH  - Glutathione/metabolism
MH  - Humans
MH  - Hydrogen Sulfide/*pharmacology
MH  - Hyperhomocysteinemia/*complications
MH  - Male
MH  - Mitochondria/*drug effects/metabolism
MH  - Mitochondrial Diseases/*drug therapy
MH  - Nitrites/metabolism
MH  - Oxidative Stress
MH  - Oxygen Consumption
MH  - Rats, Sprague-Dawley
MH  - Superoxide Dismutase/metabolism
OTO - NOTNLM
OT  - Homocysteine
OT  - Hydrogen sulfide
OT  - Mitochondria
OT  - Oxidative stress
OT  - Oxygen consumption rate
EDAT- 2019/11/22 06:00
MHDA- 2021/02/24 06:00
CRDT- 2019/11/22 06:00
PHST- 2019/03/27 00:00 [received]
PHST- 2019/08/04 00:00 [revised]
PHST- 2019/11/11 00:00 [accepted]
PHST- 2019/11/22 06:00 [pubmed]
PHST- 2021/02/24 06:00 [medline]
PHST- 2019/11/22 06:00 [entrez]
AID - S1567-7249(19)30071-6 [pii]
AID - 10.1016/j.mito.2019.11.004 [doi]
PST - ppublish
SO  - Mitochondrion. 2020 Jan;50:158-169. doi: 10.1016/j.mito.2019.11.004. Epub 2019 
      Nov 18.