This study was designed to test whether intraperitoneally injected sodium hydrosulfide (NaHS) would mimic the pulmonary alterations induced by lethal peracute exposure to an atmosphere containing hydrogen sulfide. Groups of five Sprague-Dawley rats were exposed to an atmosphere of either 2317.6 +/- 547.3 mg m-3 H2S (H2S group) or no H2S (air group), or were injected intraperitoneally with a solution containing 30 mg kg-1 sodium hydrosulfide (NaHS group) or saline solution (vehicle control). Rats of the air and saline groups were killed by cervical dislocation. All rats exposed to H2S or injected with NaHS died within 3 min; however, only rats exposed to H2S showed severe respiratory distress in the agonic phase preceding death. In addition, rats in the H2S group had a notable discharge of serous fluid from the mouth and nostrils. At necropsy, all rats in the H2S group had gross and histologic evidence of pulmonary edema characterized by massive extravasation of eosinophilic fluid into the bronchoalveolar space. In contrast, the lungs of rats injected with NaHS or saline or exposed to air were unaffected. It was concluded that the edematogenic effect of H2S in the lungs cannot be reproduced by injection of NaHS. The severity of lung edema induced by a peracute exposure to H2S was extensive enough to account for death.
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http://dx.doi.org/10.1016/0272-0590(89)90053-5 | DOI Listing |
Int J Mol Sci
January 2025
School of Life Science and Engineering, Southwest University of Science and Technology, Mianyang 621010, China.
Cadmium (Cd), as one of the most toxic nonessential elements, severely prohibits plant growth and development. Hydrogen sulfide (HS) and methyl jasmonate (MeJA) play essential roles in plant response to abiotic stress. However, the potential mechanism of HS and MeJA in alleviating Cd stress in plants remains unclear.
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January 2025
Department of Anesthesiology, Cangzhou Central Hospital, Cangzhou, China.
The potential role of hydrogen sulfide (HS) in the modulation of neuropathic pain is increasingly recognized. This study investigated the therapeutic effect of intraperitoneal injection of the HS donor sodium hydrosulfide (NaHS) on neuropathic pain. Utilizing the spared nerve injury (SNI) model in mice, the research investigates the role of astrocytes and the excitatory neurotransmitter glutamate in chronic pain.
View Article and Find Full Text PDFFood Chem
January 2025
State Key Laboratory for Conservation and Utilization of Subtropical Agro-bioresources/Guangdong Provincial Key Laboratory of Postharvest Science of Fruits and Vegetables/Engineering Research Center of Southern Horticultural Products Preservation, Ministry of Education, College of Horticulture, South China Agricultural University, Guangzhou 510642, China. Electronic address:
Sodium hydrosulfide (NaHS), a hydrogen sulfide (H₂S) donor, effectively mitigates chilling injury (CI) in bananas; however, the underlying molecular mechanisms remain unclear. This study demonstrated that NaHS alleviates CI symptoms by activating antioxidant defense systems that reduce oxidative stress induced by CI. Transcriptomic analysis revealed 1003 differentially expressed genes in three sample groups, with enrichment in pathways related to cellular processes, metabolic activity, and secondary metabolite biosynthesis.
View Article and Find Full Text PDFJCI Insight
January 2025
Center for Precision Medicine, Department of Medicine, and.
The role played by anionic channels in diabetic kidney disease (DKD) is not known. Chloride channel accessory 1 (CLCA1) facilitates the activity of TMEM16A (Anoctamin-1), a Ca2+-dependent Cl- channel. We examined if CLCA1/TMEM16A had a role in DKD.
View Article and Find Full Text PDFArch Toxicol
December 2024
State Key Laboratory of Trauma and Chemical Poisoning, Institute of Combined Injury, Chongqing Engineering Research Center for Nanomedicine, College of Preventive Medicine, Army Medical University, Chongqing, 400038, China.
Depleted uranium (DU) is a byproduct of uranium enrichment, which can cause heavy-metal toxicity and radiation toxicity as well as serious damage to the kidneys. However, the mechanism of renal injury induced by DU is still unclear. This study aimed to explore the role of ethylmalonic encephalopathy 1 (ETHE1) in DU-induced mitochondrial dysfunction and elucidate the underlying mechanisms.
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