title: Hydrogen sulfide may attenuate methylmercury-induced neurotoxicity via mitochondrial preservation.
abstract: Hydrogen sulfide (H2S) is a protective molecule and a novel gaseous mediator. Here we explored whether H2S donor (NaHS) could attenuate methylmercury (MeHg)-induced neurotoxicity in rats. The adult rats were randomly divided into four groups, i.e., control, NaHS, MeHg, and NaHS + MeHg groups. Rats of the NaHS + MeHg group were intraperitoneally (i.p) injected with 5.6 mg/kg/d of NaHS together with 5 μg/kg/d of MeHg. Rats of the MeHg group and NaHS group were injected with 5 μg/kg/d of MeHg and 5.6 mg/kg/d of NaHS, respectively. All treatments were continued for 20 d, and the cerebral cortex of the rats was evaluated. The results showed that NaHS significantly reduced MeHg-induced oxidative stress, as indicated by reduced lipid peroxide content, and increased glutathione levels and glutathione peroxidase and thioredoxin reductase activities. NaHS attenuated MeHg-induced mitochondrial damage, as indicated by increased mitochondrial activity, reduced mitochondrial swelling, and the release of cytochrome C and apoptosis-inducing factors. NaHS also decreased the number of apoptotic cells compared to that observed in MeHg only-treated rats, as indicated in a TUNEL assay. Finally, NaHS increased DNA and RNA content, and the activities of acetylcholinesterase and Na+/K+-ATPase. These indices were all lower in the MeHg group than in the control group, and NaHS alone did not observably influence any of these indices compared to the control. Our results demonstrate that H2S may protect against MeHg-induced neurotoxicity, and the mechanisms appear to involve the inhibition of oxidative stress and the protection of mitochondria.
authors.affiliation: College of Life Science and Engineering, Shenyang University, Shenyang city 110044, China.
authors.forename: Junyan
authors.initials: J
authors.lastname: Han
authors.affiliation: College of Life Science and Engineering, Shenyang University, Shenyang city 110044, China.
authors.forename: Xuelian
authors.initials: X
authors.lastname: Yang
authors.affiliation: College of Life Science and Engineering, Shenyang University, Shenyang city 110044, China.
authors.forename: Xuehua
authors.initials: X
authors.lastname: Chen
authors.affiliation: College of Life Science and Engineering, Shenyang University, Shenyang city 110044, China.
authors.forename: Zhiqiang
authors.initials: Z
authors.lastname: Li
authors.affiliation: College of Life Science and Engineering, Shenyang University, Shenyang city 110044, China.
authors.forename: Ming
authors.initials: M
authors.lastname: Fang
authors.affiliation: College of Food, Shenyang Agricultural University, Shenyang 110866, China. Electronic address: tandehongsy@126.com.
authors.forename: Bing
authors.initials: B
authors.lastname: Bai
authors.affiliation: College of Food, Shenyang Agricultural University, Shenyang 110866, China. Electronic address: baibing@hotmail.com.
authors.forename: Dehong
authors.initials: D
authors.lastname: Tan
mesh_terms: D000110:Acetylcholinesterase / Q000378:metabolism; D000818:Animals; D017209:Apoptosis / Q000187:drug effects; D051033:Apoptosis Inducing Factor / Q000378:metabolism; D002540:Cerebral Cortex / Q000187:drug effects / Q000378:metabolism; D045304:Cytochromes c / Q000378:metabolism; D005978:Glutathione / Q000378:metabolism; D005979:Glutathione Peroxidase / Q000378:metabolism; D006862:Hydrogen Sulfide / Q000494:pharmacology*; D008297:Male; D008767:Methylmercury Compounds / Q000633:toxicity*; D008928:Mitochondria / Q000187:drug effects* / Q000378:metabolism; D033681:Mitochondrial Membrane Transport Proteins / Q000187:drug effects / Q000378:metabolism; D000083162:Mitochondrial Permeability Transition Pore; D018696:Neuroprotective Agents / Q000494:pharmacology*; D018384:Oxidative Stress / Q000187:drug effects; D051381:Rats; D017207:Rats, Sprague-Dawley; D017382:Reactive Oxygen Species / Q000378:metabolism; D000254:Sodium-Potassium-Exchanging ATPase / Q000378:metabolism; D013440:Sulfides / Q000494:pharmacology; D013880:Thioredoxin-Disulfide Reductase / Q000378:metabolism
chemical_list: C494831:Aifm1 protein, rat; D051033:Apoptosis Inducing Factor; D008767:Methylmercury Compounds; D033681:Mitochondrial Membrane Transport Proteins; D000083162:Mitochondrial Permeability Transition Pore; D018696:Neuroprotective Agents; D017382:Reactive Oxygen Species; D013440:Sulfides; D045304:Cytochromes c; D005979:Glutathione Peroxidase; D013880:Thioredoxin-Disulfide Reductase; D000110:Acetylcholinesterase; D000254:Sodium-Potassium-Exchanging ATPase; C025451:sodium bisulfide; D005978:Glutathione; D006862:Hydrogen Sulfide
keywords: Acetylcholinesterase; Apoptosis; Heavy metal; Neurodegeneration; Seleno-protein