scholarly journals Production of Hydrogen Sulfide by Fermentation in Rumen and Its Impact on Health and Production of Animals

Processes ◽  
2020 ◽  
Vol 8 (9) ◽  
pp. 1169
Author(s):  
Ali Mujtaba Shah ◽  
Jian Ma ◽  
Zhisheng Wang ◽  
Rui Hu ◽  
Xueying Wang ◽  
...  
Keyword(s):  
Hydrogen Sulfide ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Animal Health ◽  
Rumen Fermentation ◽  
Intestinal Wall ◽  
Vital Role ◽  
The Body ◽  
Sulfide Concentration ◽  
Production Of Hydrogen

Hydrogen sulfide is a Janus-faced molecule with many beneficial and toxic effects on the animal health. In ruminants, rumen fermentation plays a vital role in the digestion and absorption of nutrients. During rumen fermentation, the production of hydrogen sulfide can occur, and it can be rapidly absorbed into the body of the animals through the intestinal wall. If the production of hydrogen sulfide concentration is higher in the rumen, it can cause a toxic effect on ruminants known as poliomyelitis. The production of hydrogen sulfide depends on the population of sulfate-reducing bacteria in the rumen. In rodents, H2S maintains the normal physiology of the gastrointestinal tract and also improves the healing of the chronic gastric ulcer. In the gut, H2S regulates physiological functions such as inflammation, ischemia–reperfusion injury and motility. In this review article, we summarize the toxicity occurrence in the body of animals due to high levels of hydrogen sulfide production and also recent progress in the studies of physiological function of H2S in the gut, with a special emphasis on bacteria-derived H2S is discussed in this review.

scholarly journals Role of Hydrogen Sulfide in the Endocrine System

2021 ◽  
Vol 12 ◽  
Author(s):  
Hao-Jie Chen ◽  
Ebenezeri Erasto Ngowi ◽  
Lei Qian ◽  
Tao Li ◽  
Yang-Zhe Qin ◽  
...  
Keyword(s):  
Hydrogen Sulfide ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Endocrine System ◽  
The Body ◽  
Endocrine Disorders ◽  
Hormone Concentration ◽  
Treatment Of Hypertension ◽  
Anti Inflammation

Hydrogen sulfide (H2S), as one of the three known gaseous signal transduction molecules in organisms, has attracted a surging amount of attention. H2S is involved in a variety of physiological and pathological processes in the body, such as dilating blood vessels (regulating blood pressure), protecting tissue from ischemia-reperfusion injury, anti-inflammation, carcinogenesis, or inhibition of cancer, as well as acting on the hypothalamus and pancreas to regulate hormonal metabolism. The change of H2S concentration is related to a variety of endocrine disorders, and the change of hormone concentration also affects the synthesis of H2S. Understanding the effect of biosynthesis and the concentration of H2S on the endocrine system is useful to develop drugs for the treatment of hypertension, diabetes, and other diseases.

scholarly journals Hydrogen Sulfide Prevents Ischemia-Reperfusion Injury in Muscle even when Delivered in the Post-ischemic Period

2009 ◽  
Vol 50 (4) ◽  
pp. 972
Author(s):  
P.W. Henderson ◽  
S.P. Singh ◽  
A.L. Weinstein ◽  
V. Nagineni ◽  
J.A. Spector
Keyword(s):  
Hydrogen Sulfide ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Ischemic Period

scholarly journals A Hypothesis: Hydrogen Sulfide Might Be Neuroprotective against Subarachnoid Hemorrhage Induced Brain Injury

2014 ◽  
Vol 2014 ◽  
pp. 1-9 ◽  
Author(s):  
Yong-Peng Yu ◽  
Xiang-Lin Chi ◽  
Li-Jun Liu
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Hydrogen Sulfide ◽  
Subarachnoid Hemorrhage ◽  
Brain Injury ◽  
Inflammatory Responses ◽  
Ischemia Reperfusion Injury ◽  
Leukocyte Adhesion ◽  
Ischemia Reperfusion ◽  
The Brain

Gases such as nitric oxide (NO) and carbon monoxide (CO) play important roles both in normal physiology and in disease. Recent studies have shown that hydrogen sulfide (H2S) protects neurons against oxidative stress and ischemia-reperfusion injury and attenuates lipopolysaccharides (LPS) induced neuroinflammation in microglia, exhibiting anti-inflammatory and antiapoptotic activities. The gas H2S is emerging as a novel regulator of important physiologic functions such as arterial diameter, blood flow, and leukocyte adhesion. It has been known that multiple factors, including oxidative stress, free radicals, and neuronal nitric oxide synthesis as well as abnormal inflammatory responses, are involved in the mechanism underlying the brain injury after subarachnoid hemorrhage (SAH). Based on the multiple physiologic functions of H2S, we speculate that it might be a promising, effective, and specific therapy for brain injury after SAH.

Abstract 16163: Hydrogen Sulfide Reduces Inflammasome Formation in Mice With Ischemic HFrEF

Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Adolfo G Mauro ◽  
Juan Valle Raleigh ◽  
Khoa Nguyen ◽  
David E Durrant ◽  
Erica Kim ◽  
...  
Keyword(s):  
Hydrogen Sulfide ◽  
Nlrp3 Inflammasome ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Saline Control ◽  
Lv Function ◽  
Coronary Artery Ligation ◽  
Artery Ligation ◽  
Reduced Ejection Fraction ◽  
Fractional Shortening

Background: Hydrogen sulfide (H2S) has been shown to attenuate myocardial ischemia/reperfusion injury via suppression of NOD-like receptor family, pyrin domain containing 3 (NLRP3) inflammasome. Whether the H2S donor, Na2S, protects against ischemic heart failure with reduced ejection fraction (HFrEF) when treatment is initiated after development of LV dysfunction is unknown. Methods and Results: Adult male mice underwent myocardial infarction (MI) by permanent coronary artery ligation after baseline echocardiography. Repeat echocardiography was performed at day 3 post MI and surviving mice with fractional shortening (FS) less than 25% were treated with either Na2S (100 μg/kg, ip) or saline (volume matched, ip) for 25 days. LV fractional shortening remained unchanged at 7 and 28 days post-MI in the saline group, but improved significantly with Na2S at both time points (Fig. A). Moreover, LV infarct scar size, assessed by trichrome staining, was smaller in Na2S group (14.8 ± 2.1%) as compared to control (28.8 ± 4.8%, P<0.05) at 7 days post MI. Immunofluorescence staining for apoptosis-associated speck-like protein containing a caspase recruitment domain (ASC), a component of the inflammasome, showed significant increase at 3 days post MI with sustained elevation at 7 days in the saline-treated group, whereas treatment with Na2S starting on day 3 post-MI significantly attenuated ASC 4 days later (Fig. B). Survival rate was 2-fold higher in Na2S group compared to saline control at 28 days post MI (P<0.05, Fig. C). Conclusion: Treatment with Na2S in mice with ischemic HFrEF improves LV function and survival up to 28 days post MI, possibly through suppression of ASC and prevention of further NLRP3 inflammasome formation. We propose that H2S donors can be promising therapeutic tools for ischemic HF.

scholarly journals The Cardioprotective Effects of Hydrogen Sulfide in Heart Diseases: From Molecular Mechanisms to Therapeutic Potential

2015 ◽  
Vol 2015 ◽  
pp. 1-13 ◽  
Author(s):  
Yaqi Shen ◽  
Zhuqing Shen ◽  
Shanshan Luo ◽  
Wei Guo ◽  
Yi Zhun Zhu
Keyword(s):  
Hydrogen Sulfide ◽  
Molecular Mechanisms ◽  
Inflammatory Responses ◽  
Ischemia Reperfusion Injury ◽  
Therapeutic Potential ◽  
Heart Diseases ◽  
Ischemia Reperfusion ◽  
Cardiac Diseases ◽  
Mammalian Tissues ◽  
Antioxidative Action

Hydrogen sulfide (H2S) is now recognized as a third gaseous mediator along with nitric oxide (NO) and carbon monoxide (CO), though it was originally considered as a malodorous and toxic gas. H2S is produced endogenously from cysteine by three enzymes in mammalian tissues. An increasing body of evidence suggests the involvement of H2S in different physiological and pathological processes. Recent studies have shown that H2S has the potential to protect the heart against myocardial infarction, arrhythmia, hypertrophy, fibrosis, ischemia-reperfusion injury, and heart failure. Some mechanisms, such as antioxidative action, preservation of mitochondrial function, reduction of apoptosis, anti-inflammatory responses, angiogenic actions, regulation of ion channel, and interaction with NO, could be responsible for the cardioprotective effect of H2S. Although several mechanisms have been identified, there is a need for further research to identify the specific molecular mechanism of cardioprotection in different cardiac diseases. Therefore, insight into the molecular mechanisms underlying H2S action in the heart may promote the understanding of pathophysiology of cardiac diseases and lead to new therapeutic targets based on modulation of H2S production.

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