Role Of Carbon Monoxide Research Articles

The role of carbon monoxide in the catalytic synthesis of endohedral carbyne

The unique physical properties of carbyne, a novel carbon nanostructure, have attracted considerable interest in modern nanotechnology. While carbyne synthesis has been accomplished successfully using diverse techniques, the underlying mechanisms governing the carbon monoxide-dependent catalytic synthesis of endohedral carbyne remain poorly understood. In this simulation-based study, we investigate the synthesis of endohedral carbyne from carbon and carbon monoxide radicals in the presence of a nickel catalyst inside double-walled carbon nanotubes with a (5,5)@(10,10) structure. The outcome of our investigation demonstrates that the incorporation of the carbon atom within the Nin@(5,5)@(10,10) model system initiates the formation of an elongated carbon chain. In contrast, upon the introduction of carbon monoxide radicals, the growth of the carbyne chain is inhibited as a result of the oxidation of endohedral nickel clusters by oxygen atoms after the initial steps of nucleation. Our findings align with prior theoretical, simulation, and experimental investigations, reinforcing their consistency and providing valuable insights into the synthesis of carbyne-based nanodevices that hold promising potential for future advancements in nanotechnology.

A novel red AIE fluorescent probe for ratiometric detection of carbon monoxide in vitro and in vivo.

As a significant signaling gas molecule, carbon monoxide (CO) has a crucial impact on various physiological and pathological processes in organisms, particularly in oxidative stress processes. Hence, designing and synthesizing a fluorescent probe that can effectively image CO in vivo holds immense significance. In this work, under the guidance of density functional theory (DFT) and time-dependent density functional theory (TDDFT), we designed and synthesized a red aggregation-induced emission (AIE) fluorescent probe THBTA-CO for CO detection and imaging. The fluorescent probe displayed green fluorescence emission at 535 nm before the CO response. However, upon CO response, with the involvement of Pd2+, the probe emitted red fluorescence at 630 nm. Furthermore, we successfully demonstrated the potential of THBTA-CO in visualizing both exogenous and endogenous CO in living cells. Significantly, THBTA-CO was effectively employed to image CO in lipopolysaccharide (LPS)-induced oxidative stress in mice. These findings convincingly establish THBTA-CO as a promising fluorescent probe for CO sensing and imaging, thereby facilitating a better understanding of CO's role in biomedical research.

The Role of Carbon Monoxide in the Reactions of Arterial Branches of the Uterine Artery of Rats to Low-Intensity Irradiation with a Helium-Neon Laser.

Biomicroscopy was used to study order I-IV branches of the uterine artery in sexually mature female Wistar rats after a single 5- or 10-min direct exposure of the right broad ligament of the uterus to a helium-neon laser beam in the red band of the spectrum (λ=632.8 nm, output power 2 mW, intensity 20 mW/cm2). Under the influence of laser exposure, there was a significant increase in the diameter of small uterine branches and a weaker increase in large vessels with a well-developed muscular membrane. Preliminary administration of zinc IX protoporphyrin hemoxygenase blocker (30 mmol/kg) reduced reactivity of the vascular bed to laser irradiation, mainly of order I-II branches. It was concluded that carbon monoxide can act as an intermediary between the laser exposure and uterine vessels.

Role of Carbon Monoxide in Oxidative Stress-Induced Senescence in Human Bronchial Epithelium.

Prolonged or excessive stimulation from inhaled toxins may cause oxidative stress and DNA damage that can lead to stress-induced senescence in epithelial cells, which can contribute to several airway diseases. Mounting evidence has shown carbon monoxide (CO) confers cytoprotective effects. We investigated the effects of CO on oxidative stress-induced senescence in human airway epithelium and elucidated the underlying molecular mechanisms. Here, CO pretreatment reduced H2O2-mediated increases in total reactive oxygen species (ROS) production and mitochondrial superoxide in a human bronchial epithelial cell line (BEAS-2B). H2O2 treatment triggered a premature senescence-like phenotype with enlarged and flattened cell morphology accompanied by increased SA-β-gal activity, cell cycle arrest in G0/G1, reduced cell viability, and increased transcription of senescence-associated secretory phenotype (SASP) genes. Additionally, exposure to H2O2 increased protein levels of cellular senescence markers (p53 and p21), reduced Sirtuin 3 (SIRT3) and manganese superoxide dismutase (MnSOD) levels, and increased p53 K382 acetylation. These H2O2-mediated effects were attenuated by pretreatment with a CO-containing solution. SIRT3 silencing induced mitochondrial superoxide production and triggered a senescence-like phenotype, whereas overexpression decreased mitochondrial superoxide production and alleviated the senescence-like phenotype. Air-liquid interface (ALI) culture of primary human bronchial cells, which becomes a fully differentiated pseudostratified mucociliary epithelium, was used as a model. We found that apical and basolateral exposure to H2O2 induced a vacuolated structure that impaired the integrity of ALI cultures, increased goblet cell numbers, decreased SCGB1A1+ club cell numbers, increased p21 protein levels, and increased SASP gene transcription, consistent with our observations in BEAS-2B cells. These effects were attenuated in the apical presence of a CO-containing solution. In summary, we revealed that CO has a pivotal role in epithelial senescence by regulating ROS production via the SIRT3/MnSOD/p53/p21 pathway. This may have important implications in the prevention and treatment of age-associated respiratory pathologies.

Microbial conversion of syngas to single cell protein: The role of carbon monoxide

Syngas has been widely utilized as substrate in microbial processes to produce various high-value products. Nevertheless, its applicability for single cell protein (SCP) production by hydrogen-oxidizing bacteria (HOB) has never been explored. Especially, the role of carbon monoxide in SCP synthesis is unknown. Thus, this study first investigated the effect of different CO and H2 ratios in syngas on Cupriavidus necator H16 growth and SCP production. The growth of C. necator H16 was significantly restrained with the increase of CO content, and it almost ceased once the CO:H2 ratios were above 1. In addition, the growth rate of C. necator H16 increased with the increase of shaking frequency and inoculum volume. Furthermore, larger gas–liquid interfacial areas and gas input amount resulted in a higher growth rate and OD value. The raw protein contents were around 50–60% regardless of CO concentration, and the amino acid profiles showed no apparent differences. The results showed that although the presence of CO led to the reduction of the growth rate of C. necator H16, it had a limited effect on the SCP quality. H2 and CO2 in syngas were the primary substrates for SCP production, while CO served more as a toxic inhibitor. The successful demonstration of SCP synthesis from syngas may provide a superior route for the valorization of waste biomass by turning it into food or feed.

The Role of Carbon Monoxide and Their Donor (CORM-2) in Skin Wound Healing in Mice

Carbon monoxide, which is a toxic gas, has a beneficial effect on cells in low doses. It is known that low concentrations of this gas are produced in the body during the decay of heme-containing proteins and have pro-apoptotic, anti-inflammatory, anti-allergic, vasodilator effects, stimulating angiogenesis. The danger of using this gas is the difficulty of its dosage. CO donors are used to controlling the amount and gradual release of carbon monoxide. This study studied the effect of treatment with CO and donor CORM-2 on wound healing processes in laboratory mice. Treatment with CO and CORM-2 reduced the healing rate of skin wounds in laboratory mice. The greatest delay in healing was observed in animals whose wounds were treated with CO. In this group, aquaporin-3 mRNA expression was decreased to the smallest degree among all other animals. This most likely caused the appearance of crusts. CORM-2 treatment also led to a decrease in AQP3 mRNA expression, but no crusts were formed. This can be explained by the fact that CO is released slowly. Having a dry crust on the wound increases the healing time. But, the formation of a dry crust is useful in the healing of burns, because with a dry scab, pus cannot appear; with some degrees of burns, it prevents suppuration and creates a protective barrier. The study confirmed the hypothesis that CO and CORM-2 reduce AQP3 expression after treatment of damaged skin.

Triton Haze Analogs: The Role of Carbon Monoxide in Haze Formation

AbstractTriton is the largest moon of the Neptune system and possesses a thin nitrogen atmosphere with trace amounts of carbon monoxide and methane, making it of similar composition to that of the dwarf planet Pluto. Like Pluto and Saturn's moon Titan, Triton has a haze layer thought to be composed of organics formed through photochemistry. Here, we perform atmospheric chamber experiments of 0.5% CO and 0.2% CH4 in N2 at 90 K and 1 mbar to generate Triton haze analogs. We then characterize the physical and chemical properties of these particles. We measure their production rate, their bulk composition with combustion analysis, their molecular composition with very high resolution mass spectrometry, and their transmission and reflectance from the optical to the near‐infrared with Fourier Transform Infrared (FTIR) Spectroscopy. We compare these properties to existing measurements of Triton's tenuous atmosphere and surface, as well as contextualize these results in view of all the small, hazy, nitrogen‐rich worlds of our solar system. We find that carbon monoxide present at greater mixing ratios than methane in the atmosphere can lead to significantly oxygen‐ and nitrogen‐rich haze materials. These Triton haze analogs have clear observable signatures in their near‐infrared spectra, which may help us differentiate the mechanisms behind haze formation processes across diverse solar system bodies.

Devil or angel: two roles of carbon monoxide in stroke.

Stroke is one of the most important acute diseases that endanger human health and result in death, including acute cerebral hemorrhage and acute cerebral ischemia. Acute onset is its most prominent feature. Carbon monoxide (CO) is a colorless and odorless gas existing at room temperature. It is not only a common air pollutant, but also has been found to be closely related to stroke. A large amount of exogenous CO has an important impact on the incidence and prognosis of stroke, while endogenous CO as a gas signal also has an important impact on neuroprotection after stroke. Both low-dose CO inhalation and CO-releasing molecule-3 (a molecule that emits CO) treatment have shown the benefits of stroke, and perhaps the role of CO in stroke is one of the key areas for future research.

Modulatory Role of Carbon Monoxide on the Inflammatory Response and Oxidative Stress Linked to Gastrointestinal Disorders.

Significance: Carbon monoxide (CO) is an endogenous gaseous mediator that plays an important role in maintaining gastrointestinal (GI) tract homeostasis, acting in mucosal defense, and providing negative modulation of pathophysiological markers of clinical conditions. Recent Advances: Preclinical studies using animal models and/or cell culture show that CO can modulate the inflammatory response and oxidative stress in GI mucosal injuries and pathological conditions, reducing proinflammatory cytokines and reactive oxygen species, while increasing antioxidant defense mechanisms. Critical Issues: CO has potent anti-inflammatory and antioxidant effects. The defense mechanisms of the GI tract are subject to aggression by different chemical agents (e.g., drugs and ethanol) as well as complex and multifactorial diseases, with inflammation and oxidative stress as strong triggers for the deleterious effects. Thus, it is possible that CO acts on a variety of molecules involved in the inflammatory and oxidative signaling cascades, as well as reinforcing several defense mechanisms that maintain GI homeostasis. Future Directions: CO-based therapies are promising tools for the treatment of GI disorders, such as gastric and intestinal injuries, inflammatory bowel disease, and pancreatitis. Therefore, it is necessary to develop safe and selective CO-releasing agents and/or donor drugs to facilitate effective treatments and methods for analysis of CO levels that are simple and inexpensive. Antioxid. Redox Signal. 37, 98-114.

Heme oxygenase‑1 improves the survival of ischemic skin flaps (Review).

Heat shock protein 32 (Hsp32), also known as heme oxygenase-1 (HO-1), is an enzyme that exists in microsomes. HO-1 can be induced by a variety of stimuli, including heavy metals, heat shock, inflammatory stimuli, heme and its derivatives, stress, hypoxia, and biological hormones. HO-1 is the rate-limiting enzyme of heme catabolism, which splits heme into biliverdin, carbon monoxide (CO) and iron. The metabolites of HO-1 have anti-inflammatory and anti-oxidant effects, and provide protection to the cardiovascular system and transplanted organs. This review summarizes the biological characteristics of HO-1 and the functional significance of its products, and specifically elaborates on its protective effect on skin flaps. HO-1 improves the survival rate of ischemic skin flaps through anti-inflammatory, anti-oxidant and vasodilatory effects of enzymatic reaction products. In particular, this review focuses on the role of carbon monoxide (CO), one of the primary metabolites of HO-1, in flap survival and discusses the feasibility and existing challenges of HO-1 in flap surgery.

Topical application of CNTF, GDNF and BDNF in combination attenuates blood-spinal cord barrier permeability, edema formation, hemeoxygenase-2 upregulation, and cord pathology.

Spinal cord injury (SCI) is one of the leading causes of disability in Military personnel for which no suitable therapeutic strategies are available till today. Thus, exploration of novel therapeutic measures is highly needed to enhance the quality of life of SCI victims. Previously, topical application of BDNF and GDNF in combination over the injured spinal cord after 90min induced marked neuroprotection. In present investigation, we added CNTF in combination with BDNF and/or GDNF treatment to examine weather the triple combination applied over the traumatic cord after 90 or 120min could thwart cord pathology. Since neurotrophins attenuate nitric oxide (NO) production in SCI, the role of carbon monoxide (CO) production that is similar to NO in inducing cell injury was explored using immunohistochemistry of the constitutive isoform of enzyme hemeoxygenase-2 (HO-2). SCI inflicted over the right dorsal horn of the T10-11 segments by making an incision of 2mm deep and 5mm long upregulated the HO-2 immunostaining in the T9 and T12 segments after 5h injury. These perifocal segments are associated with breakdown of the blood-spinal cord barrier (BSCB), edema development and cell injuries. Topical application of CNTF with BDNF and GDNF in combination (10ng each) after 90 and 120min over the injured spinal cord significantly attenuated the BSCB breakdown, edema formation, cell injury and overexpression of HO-2. These observations are the first to show that CNTF with BDNF and GDNF induced superior neuroprotection in SCI probably by downregulation of CO production, not reported earlier.

Role of Carbon Monoxide in Host-Gut Microbiome Communication.

Nature is full of examples of symbiotic relationships. The critical symbiotic relation between host and mutualistic bacteria is attracting increasing attention to the degree that the gut microbiome is proposed by some as a new organ system. The microbiome exerts its systemic effect through a diverse range of metabolites, which include gaseous molecules such as H2, CO2, NH3, CH4, NO, H2S, and CO. In turn, the human host can influence the microbiome through these gaseous molecules as well in a reciprocal manner. Among these gaseous molecules, NO, H2S, and CO occupy a special place because of their widely known physiological functions in the host and their overlap and similarity in both targets and functions. The roles that NO and H2S play have been extensively examined by others. Herein, the roles of CO in host-gut microbiome communication are examined through a discussion of (1) host production and function of CO, (2) available CO donors as research tools, (3) CO production from diet and bacterial sources, (4) effect of CO on bacteria including CO sensing, and (5) gut microbiome production of CO. There is a large amount of literature suggesting the "messenger" role of CO in host-gut microbiome communication. However, much more work is needed to begin achieving a systematic understanding of this issue.

The role of carbon monoxide, heme oxygenase 1, and the Nrf2 transcription factor in the modulation of chronic pain and their interactions with opioids and cannabinoids.

Chronic pain and its associated comorbidities are difficult to treat, even when the most potent analgesic compounds are used. Thus, research on new strategies to effectively relieve nociceptive and/or emotional disorders accompanying chronic pain is essential. Several studies have demonstrated the anti-inflammatory and antinociceptive effects of different carbon monoxide-releasing molecules (CO-RMs), inducible heme oxygenase 1 (HO-1), and nuclear factor-2 erythroid factor-2 (Nrf2) transcription factor activators in several models of acute and chronic pain caused by inflammation, nerve injury or diabetes. More recently, the antidepressant and/or anxiolytic effects of several Nrf2 transcription factor inducers were demonstrated in a model of chronic neuropathic pain. These effects are mainly produced by inhibition of oxidative stress, inflammation, glial activation, mitogen-activated protein kinases and/or phosphoinositide 3-kinase/phospho-protein kinase B phosphorylation in the peripheral and/or central nervous system. Other studies also demonstrated that the analgesic effects of opioids and cannabinoids are improved when these drugs are coadministered with CO-RMs, HO-1 or Nrf2 activators in different preclinical pain models and that these improvements are generally mediated by upregulation or prevention of the downregulation of µ-opioid receptors, δ-opioid receptors and/or cannabinoid 2 receptors in the setting of chronic pain. We reviewed all these studies as well as studies on the mechanisms of action underlying the effects of CO-RMs, HO-1, and Nrf2 activators in chronic pain. In summary, activation of the Nrf2/HO-1/carbon monoxide signaling pathway alone and/or in combination with the administration of specific analgesics is a valid strategy for the treatment of chronic pain and some associated emotional disorders.

Carbon monoxide-releasing molecule-3: Amelioration of renal ischemia reperfusion injury in a rat model.

PurposeDespite the role of carbon monoxide in ameliorating ischemia-reperfusion injury (IRI), its use in the clinical setting is restricted owing to its toxicity. Herein, we investigated the in vivo effects of carbon monoxide–releasing molecule-3 (CORM-3) on IRI.Materials and MethodsFifteen rats were equally and randomly divided into three groups: sham (right nephrectomy), control (right nephrectomy and left renal ischemia), and CORM-3 (right nephrectomy and CORM-3 injection before left renal ischemia). Kidney tissues and blood samples collected from sacrificed rats were evaluated to determine the renoprotective effect and mechanism of CORM-3.ResultsConcentrations of serum creatinine and kidney injury molecule-1 in the CORM-3 group were significantly lower than in the control group after 75 minutes of IRI (1.2 vs. 2.4 mg/dL, p=0.01, and 292 vs. 550 pg/mL, p<0.001, respectively). Furthermore, the CORM-3 group exhibited a higher portion of normal tubules and glomeruli. TUNEL staining revealed fewer apoptotic renal tubular cells in the CORM-3 group than in the control group. The expression of 960 genes in the CORM-3 group was also altered. Pretreatment with CORM-3 before renal IRI produced a significant renoprotective effect. Fifteen of the altered genes were found to be involved in the peroxisome proliferator-activated receptors signaling pathway, and the difference in the expression of these genes between the CORM-3 and control groups was statistically significant (p<0.001).ConclusionsCORM-3 ameliorates IRI by decreasing apoptosis and may be a novel strategy for protection against renal warm IRI.

Role of Carbon Monoxide in the Mechanisms of Action of Extracellular ATP on Contractile Activity of Vascular Smooth Muscle Cells.

We studied the role of carbon monoxide (CO) in the effect of P2X and P2Y receptor agonist ATP on the tone of rat aorta segments with intact endothelium. ATP (1-1000 μM) and P2X receptor agonist α,β-MeATP (100 μM) relaxed segments precontracted with phenylephrine (10 μM), while UTP (100-1000 μM) increased the amplitude of phenylephrine-induced contraction. The relaxing effect of ATP was enhanced by CORM II (100 μM), NO synthase inhibitor L-NAME, and guanylate cyclase inhibitor ODQ and attenuated by ZnPP IX (100 μM). The constrictive effect of UTP was weakened by CORM II (100 μM), but was not changed by ZnPP IX (100 μM). ZnPP IX (100 μM) weakened the relaxation response to α,β-MeATP. Thus, ATP involves the CO-dependent signaling cascade through P2X receptors.

Novel Role of Carbon Monoxide in Improving Neurological Outcome After Cardiac Arrest in Aged Rats: Involvement of Inducing Mitochondrial Autophagy.

BackgroundDysfunctional mitochondria are associated with neurological injury after cardiac arrest (CA). Although carbon monoxide (CO) has shown various potential therapeutic effects in preclinical tissue injury models, its mechanism of action in CA remains unclear. We sought to investigate the effects of a novel CO‐releasing molecule on cerebral mitochondrial dysfunction and neurological injury after CA.Methods and ResultsMale Sprague‐Dawley rats aged 20 to 22 months were subjected to 6‐minute asphyxia CA before receiving CO treatment. Survival, neurologic deficit scores, neuronal death, mitochondrial function, and autophagy were evaluated after the return of spontaneous circulation. Results showed that CO post‐treatment increased 3‐day survival rate from 25% to 70.83% and reduced neurologic deficit scores. CO also ameliorated CA‐induced neuronal apoptosis and necrosis in the cerebral cortex and improved cerebral mitochondrial function by reducing reactive oxygen species, reversing mitochondrial membrane potential depolarization, and preventing cytochrome C release. Furthermore, CO increased mitochondrial autophagy by inducing mitochondrial accumulation of PINK1 (PTEN‐induced putative kinase 1) and Parkin. Downregulation of PINK1 with genetic silencing siRNA abolished CO‐afforded mitochondrial autophagy.ConclusionsTaken together, our results indicate, for the first time, that CO treatment confers neuroprotection against ischemic neurological injury after CA possibly by promoting mitochondrial autophagy.

Resveratrol protects UVB‐irradiated keratinocytes by upregulating HO‐1 expression and improving mitochondrial function via endogenous CO signaling

Excessive exposure to ultraviolet (UV) radiation has been reported to promote uncontrolled reactive oxygen species (ROS) production, particularly in the mitochondria, and thus implicated in the prevalence of skin injuries. Considering the antioxidative effect of resveratrol (RES) in reducing UV‐induced ROS production in human keratinocytes (HaCaT cells) and the role of carbon monoxide (CO) in regulating oxidative stress, we hypothesized that RES may promote cellular antioxidant response by activating heme oxygenase‐1 (HO‐1) which can generate its enzymatic product, CO, in UVB‐irradiated keratinocytes. To test our hypothesis, we treated HaCaT cells with CO‐releasing molecule 2 (CORM‐2) (source of CO) and RES either independently or in combination and irradiated the cells with UVB. Co‐treatment of CO with RES upregulated HO‐1 expression and subsequently reduced intracellular ROS in response to UV irradiation. Moreover, UVB treatment alone induced mitochondrial biogenesis, but treatment with CO and RES did not increase it further. With UVB treatment, RES showed enhanced mitochondrial respiration while CO did not instigate any effect; however, independent or co‐treatment mitigated mitochondrial ROS production. Taken together, our data support the impression that endogenous CO generated from RES‐mediated activation of HO‐1 may play a crucial role in cellular antioxidant response and mitochondrial function.Support or Funding InformationThis work was supported by the Korea Institute of Planning and Evaluation for Technology in Food, Agriculture, Forestry, and Fisheries (IPET) through the High Value‐Added Food Technology Development Program, funded by the Ministry of Agriculture, Food, and Rural Affairs (Grant No. 116026‐03‐2‐HD020), Republic of Korea.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Carbon monoxide releasing molecule-3 alleviates neuron death after spinal cord injury via inflammasome regulation.

BackgroundGenetic overexpression or pharmacological activation of heme oxygenase (HO) are identified as potential therapeutic target for spinal cord injury (SCI); however, the role of carbon monoxide (CO), which is a major product of haem degenerated by HO, in SCI remains unknown. Applying hemin or chemicals which may regulate HO expression or activity to increase CO production are inadequate to elaborate the direct role of CO. Here, we assessed the effect of CO releasing molecule-3 (CORM-3), the classical donor of CO, in SCI and explained its possible protective mechanism.MethodsRat SCI model was performed with a vascular clip (30 g) compressing at T9 vertebral level for 1 min and CO was delivered immediately after SCI by CORM-3. The neurological deficits and neuron survival were assessed. Inflammasome and inositol-requiring enzyme 1 (IRE1) pathway were measured by western blot and immunofluorescence. For in vitro study, oxygen glucose deprivation (OGD) simulated the SCI-inflammasome change in cultured the primary neurons.FindingsCORM-3 suppressed inflammasome signaling and pyroptosis occurrence, which consequently alleviated neuron death and improved motor functional recovery following SCI. As a pivotal sensor involving in endoplasmic reticulum stress-medicated inflammasome signaling, IRE1 and its downstream X-box binding protein 1 (XBP1) were activated in SCI tissues as well as in OGD neurons; while inhibition of IRE1 by STF-083010 in SCI rats or by si-RNA in OGD neurons suppressed inflammasome signaling and pyroptosis. Interestingly, the SCI/OGD-stimulated IRE1 activation was attenuated by CORM-3 treatment.InterpretationsCO may alleviate neuron death and improve motor functional recovery in SCI through IRE1 regulation, and administration of CO could be a promising therapeutic strategy for SCI.

УЧАСТИЕ МОНООКСИД УГЛЕРОДА В КОРРЕКЦИИ РЕПЕРФУЗИОНЫХ ПОВРЕЖДЕНИЙ ПЕЧЕНИ

Reperfusion liver injuries are common in clinical practice during hepatic transplantation, resections or traumas&nbsp;when temporary occlusion of the main vessels (Pringle's maneuver) of the organ is necessary. The purpose of the&nbsp;review is to analyze and summarize our own and literature data about the role of carbon monoxide in the development&nbsp;and correction of hepatic ischemia-reperfusion syndrome in an experiment.

Role of Carbon Monoxide in Traumatic Brain Injury Repair

Role of Carbon Monoxide in Traumatic Brain Injury Repair