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Cardiovascular regulation of tissue oxygenation is generally viewed as an anti-drop process that prevents tissue oxygen concentration from falling below some minimum. I propose that cardiovascular regulation is predominately an anti-rise process designed to downregulate oxygen delivery. This maintains an evolutionarily conserved, reduced intracellular environment to prevent oxidation of redox-sensitive regulatory protein thiols. A number of points support this hypothesis. First, oxygen is the only nutrient with a positive, fourfold diffusion gradient from the environment to systemic tissues, minimizing the likelihood that oxygen delivery is limited. Second, hemoglobin (Hb) retains oxygen unless offloading is absolutely necessary. The allosteric properties of Hb keep oxygen tightly bound until absolutely needed, and the Bohr shift, which favors offloading, is only transient and lost when metabolism is restored. Third, a myoglobin-like Hb (xHb) would offload all of its oxygen and could easily have evolved, but it did not. Fourth, oxygen-sensitive vasoconstrictors and hyperoxic-rarefaction prevent acute and chronic over perfusion. Fifth, Fåhraeus and Fåhraeus-Lindqvist effects reduce capillary hematocrit to minimize microcirculatory oxygen content. Sixth, venous blood remains 75% saturated, wasting 75% of cardiac output were an oxygen reserve not needed. Finally, xHb-containing red blood cells could be considerably smaller and thereby decrease Fåhraeus and Fåhraeus-Lindqvist effects and cardiac load. In summary, the capacity of the cardiovascular system to deliver oxygen to the tissues generally exceeds demand, and although maintenance of an oxygen delivery reserve is important, it is more important to prevent excess oxygen delivery. [ABSTRACT FROM AUTHOR]

Naphthoquinone (1,4-NQ) and its derivatives (NQs, juglone, plumbagin, 2-methoxy-1,4-NQ, and menadione) have a variety of therapeutic applications, many of which are attributed to redox cycling and the production of reactive oxygen species (ROS). We previously demonstrated that NQs also oxidize hydrogen sulfide (H2S) to reactive sulfur species (RSS), potentially conveying identical benefits. Here we use RSS-specific fluorophores, mass spectroscopy, EPR and UV-Vis spectrometry, and oxygen-sensitive optodes to examine the effects of thiols and thiol-NQ adducts on H2S-NQ reactions. In the presence of glutathione (GSH) and cysteine (Cys), 1,4-NQ oxidizes H2S to both inorganic and organic hydroper-/hydropolysulfides (R2Sn, R=H, Cys, GSH; n = 2–4) and organic sulfoxides (GSnOH, n = 1, 2). These reactions reduce NQs and consume oxygen via a semiquinone intermediate. NQs are also reduced as they form adducts with GSH, Cys, protein thiols, and amines. Thiol, but not amine, adducts may increase or decrease H2S oxidation in reactions that are both NQ- and thiol-specific. Amine adducts also inhibit the formation of thiol adducts. These results suggest that NQs may react with endogenous thiols, including GSH, Cys, and protein Cys, and that these adducts may affect both thiol reactions as well as RSS production from H2S. [ABSTRACT FROM AUTHOR]

Significance: Nutraceuticals are ingested for health benefits, in addition to their general nutritional value. These dietary supplements have become increasingly popular since the late 20th century and they are a rapidly expanding global industry approaching a half-trillion U.S. dollars annually. Many nutraceuticals are promulgated as potent antioxidants. Recent Advances: Experimental support for the efficacy of nutraceuticals has lagged behind anecdotal exuberance. However, accumulating epidemiological evidence and recent, well-controlled clinical trials are beginning to support earlier animal and in vitro studies. Although still somewhat limited, encouraging results have been suggested in essentially all organ systems and against a wide range of pathophysiological conditions. Critical Issues: Health benefits of "antioxidant" nutraceuticals are largely attributed to their ability to scavenge oxidants. This has been criticized based on several factors, including limited bioavailability, short tissue retention time, and the preponderance of endogenous antioxidants. Recent attention has turned to nutraceutical activation of downstream antioxidant systems, especially the Keap1/Nrf2 (Kelch like ECH associated protein 1/nuclear factor erythroid 2-related factor 2) axis. The question now becomes, how do nutraceuticals activate this axis? Future Directions: Reactive sulfur species (RSS), including hydrogen sulfide (H2S) and its metabolites, are potent activators of the Keap1/Nrf2 axis and avid scavengers of reactive oxygen species. Evidence is beginning to accumulate that a variety of nutraceuticals increase cellular RSS by directly providing RSS in the diet, or through a number of catalytic mechanisms that increase endogenous RSS production. We propose that nutraceutical-specific targeting of RSS metabolism will lead to the design and development of even more efficacious antioxidant therapeutic strategies. Antioxid. Redox Signal. 38, 68–94. [ABSTRACT FROM AUTHOR]

1,4-Napththoquinones (NQs) are clinically relevant therapeutics that affect cell function through production of reactive oxygen species (ROS) and formation of adducts with regulatory protein thiols. Reactive sulfur species (RSS) are chemically and biologically similar to ROS and here we examine RSS production by NQ oxidation of hydrogen sulfide (H2S) using RSS-specific fluorophores, liquid chromatography-mass spectrometry, UV-Vis absorption spectrometry, oxygen-sensitive optodes, thiosulfate-specific nanoparticles, HPLC-monobromobimane derivatization, and ion chromatographic assays. We show that NQs, catalytically oxidize H2S to per- and polysulfides (H2Sn, n = 2–6), thiosulfate, sulfite and sulfate in reactions that consume oxygen and are accelerated by superoxide dismutase (SOD) and inhibited by catalase. The approximate efficacy of NQs (in decreasing order) is, 1,4-NQ ≈ juglone ≈ plumbagin > 2-methoxy-1,4-NQ ≈ menadione >> phylloquinone ≈ anthraquinone ≈ menaquinone ≈ lawsone. We propose that the most probable reactions are an initial two-electron oxidation of H2S to S0 and reduction of NQ to NQH2. S0 may react with H2S or elongate H2Sn in variety of reactions. Reoxidation of NQH2 likely involves a semiquinone radical (NQ·−) intermediate via several mechanisms involving oxygen and comproportionation to produce NQ and superoxide. Dismutation of the latter forms hydrogen peroxide which then further oxidizes RSS to sulfoxides. These findings provide the chemical background for novel sulfur-based approaches to naphthoquinone-directed therapies. [ABSTRACT FROM AUTHOR]

In the canonical pathway for mitochondrial H 2 S oxidation electrons are transferred from sulfide:quinone oxidoreductase (SQR) to complex III via ubiquinone (CoQ 10). We previously observed that a number of quinones directly oxidize H 2 S and we hypothesize that CoQ 10 may have similar properties. Here we examine H 2 S oxidation by CoQ 10 and more hydrophilic, truncated forms, CoQ 1 and CoQ 0 , in buffer using H 2 S and polysulfide fluorophores (AzMC and SSP4), silver nanoparticles to measure thiosulfate (H 2 S 2 O 3), mass spectrometry to identify polysulfides and O 2 -sensitive optodes to measure O 2 consumption. We show that all three quinones concentration-dependently catalyze the oxidization of H 2 S to polysulfides and thiosulfate in buffer with the potency CoQ 0 >CoQ 1 >CoQ 10 and that CoQ 0 specifically oxidizes H 2 S to per-polysulfides, H 2 S 2,3,4. These reactions consume and require oxygen and are augmented by addition of SOD suggesting that the quinones, not superoxide, oxidize H 2 S. Related quinones, MitoQ, menadione and idebenone, oxidize H 2 S in similar reactions. Exogenous CoQ 0 decreases cellular H 2 S and increases polysulfides and thiosulfate production and this is also O 2 -dependent, suggesting that the quinone has similar effects on sulfur metabolism in cells. Collectively, these results suggest an additional endogenous mechanism for H 2 S metabolism and a potential therapeutic approach in H 2 S-related metabolic disorders. Role of ubiquinone in H 2 S oxidation. (A) In the initial step of the canonical pathway, mitochondrial sulfide:quinone oxidoreductase (SQR) oxidizes H 2 S and the electrons are transferred to the electron transport chain (ETC) complex III via ubiquinone (Q) and then to complex IV by cytochrome C (C), ultimately reducing oxygen. The persulfide formed from H 2 S-SQR is transferred to a mobile carrier such as glutathione (GS−) and is ultimately oxidized to sulfate. (B) H 2 S can also be directly oxidized by mitochondrial and/or extramitochondrial ubiquinone in a reaction that produces polysulfides and thiosulfate and consumes oxygen but does not deliver electrons to the ETC. This pathway may serve to produce signaling polysulfides or remove H 2 S without generating ATP. [Display omitted] • Para-quinones oxidize H 2 S to polysulfides. • Ubiquinone (CoQ10), CoQ1, CoQ0, MitoQ, menadione and idebenone are para-quinones. • All oxidize H 2 S to polysulfides. • Polysulfides are potent antioxidants. • Regulation of sulfur metabolism is a promising target of antioxidant therapies. [ABSTRACT FROM AUTHOR]

Nutraceutical polyphenol catechins in green tea oxidize H 2 S to polysulfides (PS) in buffer and in cells thereby conveying their cytoprotective effects. Here we measure H 2 S oxidation in buffer and HEK293 cells by over-the-counter nutraceuticals, blueberry, bilberry and cranberry, and by polyphenols, cyanadin (Cya), quercetin (Que), rosmarinic acid (RA) and resveratrol (Res). H 2 S and PS were measured with specific fluorophores, AzMc and SSP4 respectively, and thiosulfate (TS) production was measured in buffer using silver nanoparticles (AgNPs). All compounds increased polysulfide production from H 2 S in buffer and increased polysufides in cells. Decreasing oxygen from 100% to 21% and 0% progressively decreased PS production by Que and RA in buffer and Que decreased PS production in cells incubated in 5% O 2 compared to 21% O 2. Que, RA and Res, but not Cya, increased TS production from H 2 S in 21% O 2 but not in 0% O 2. Superoxide dismutase did not affect PS production from H 2 S by Que or TS production from H 2 S by Que, RA or Res, whereas catalase inhibited TS production by all three polyphenols. Conversely, these polyphenols only slightly reduce a mixed polysulfide (K 2 S n) or thiosulfate to H 2 S in 0% O 2. Collectively, our results suggest that polyphenols are autoxidized to a semiquinone radical and that this, in turn, oxidizes H 2 S to a thiyl radical from which polysulfides and thiosulfate derived. They also suggest that this is catalyzed by a semiquinone radical and it is independent of either superoxide or hydrogen peroxide concomitantly produced during polyphenol autoxidation. The polysulfides produced in these reactions are potent antioxidants and also initiate a variety of downstream cytoprotective effector mechanisms. It is also possible that H 2 S can be regenerated from the thiosulfate produced in these reactions by other cellular reductants and reused in subsequent reactions. [Display omitted] • Health benefits of nutraceutical polyphenols (NP) are attributed to their antioxidant activity. • Autoxidation of NPs produces oxidative semiquinones. • Semiquinones oxidize hydrogen sulfide (H 2 S) to polysulfides. • Polysulfides are potent antioxidants and activate antioxidant effector mechanisms. • We propose that many health benefits of NPs are mediated by sulfur metabolism. [ABSTRACT FROM AUTHOR]

Significance: Oxidative stress in moderation positively affects homeostasis through signaling, while in excess it is associated with adverse health outcomes. Both activities are generally attributed to reactive oxygen species (ROS); hydrogen peroxide as the signal, and cysteines on regulatory proteins as the target. However, using antioxidants to affect signaling or benefit health has not consistently translated into expected outcomes, or when it does, the mechanism is often unclear. Recent Advances: Reactive sulfur species (RSS) were integral in the origin of life and throughout much of evolution. Sophisticated metabolic pathways that evolved to regulate RSS were easily "tweaked" to deal with ROS due to the remarkable similarities between the two. However, unlike ROS, RSS are stored, recycled, and chemically more versatile. Despite these observations, the relevance and regulatory functions of RSS in extant organisms are generally underappreciated. Critical Issues: A number of factors bias observations in favor of ROS over RSS. Research conducted in room air is hyperoxic to cells, and promotes ROS production and RSS oxidation. Metabolic rates of rodent models greatly exceed those of humans; does this favor ROS? Analytical methods designed to detect ROS also respond to RSS. Do these disguise the contributions of RSS? Future Directions: Resolving the ROS/RSS issue is vital to understand biology in general and human health in particular. Improvements in experimental design and analytical methods are crucial. Perhaps the most important is an appreciation of all the attributes of RSS and keeping an open mind. [ABSTRACT FROM AUTHOR]

Aim: Numerous studies have shown that H2S serves as an acute oxygen sensor in a variety of cells. We hypothesize that H2S also serves in extended oxygen sensing. Methods: Here, we compare the effects of extended exposure (24‐48 hours) to varying O2 tensions on H2S and polysulphide metabolism in human embryonic kidney (HEK 293), human adenocarcinomic alveolar basal epithelial (A549), human colon cancer (HTC116), bovine pulmonary artery smooth muscle, human umbilical‐derived mesenchymal stromal (stem) cells and porcine tracheal epithelium (PTE) using sulphur‐specific fluorophores and fluorometry or confocal microscopy. Results: All cells continuously produced H2S in 21% O2 and H2S production was increased at lower O2 tensions. Decreasing O2 from 21% to 10%, 5% and 1% O2 progressively increased H2S production in HEK293 cells and this was partially inhibited by a combination of inhibitors of H2S biosynthesis, aminooxyacetate, propargyl glycine and compound 3. Mitochondria appeared to be the source of much of this increase in HEK 293 cells. H2S production in all other cells and PTE increased when O2 was lowered from 21% to 5% except for HTC116 cells where 1% O2 was necessary to increase H2S, presumably reflecting the hypoxic environment in vivo. Polysulphides (H2Sn, where n = 2‐7), the key signalling metabolite of H2S also appeared to increase in many cells although this was often masked by high endogenous polysulphide concentrations. Conclusion: These results show that cellular H2S is increased during extended hypoxia and they suggest this is a continuously active O2‐sensing mechanism in a variety of cells. [ABSTRACT FROM AUTHOR]

The health benefits of lipoic acid (LA) are generally attributed to mitigating the harmful effects of reactive oxygen species (ROS). ROS are chemically similar to reactive sulfur species (RSS) and signal through identical mechanisms. Here we examined the effects of LA on RSS in HEK293 cells using H 2 S and polysulfide (PS) specific fluorophores, AzMC and SSP4. We show that LA concentration-dependently increased both H 2 S and PS. Physioxia (5% O 2) augmented the effects of LA on H 2 S production but decreased PS production. Thiosulfate, a known substrate for reduced LA, and an intermediate in the catabolism of H 2 S enhanced the effects of LA on H 2 S and PS production. Inhibiting peroxiredoxins with conoidin A and gluraredoxins with tiopronin augmented the effects of LA on PS and H 2 S, respectively while decreasing glutathione with buthionine-sulfoximine (BSO) or diethyl maleate (DEM) decreased the stimulatory effect of LA on H 2 S production but augmented LA's effect on PS. Aminooxyacetate (AOA) and propargylglycine (PPG), inhibitors of H 2 S production from cysteine partially inhibited LA augmentation of H 2 S production and further decreased the LA effect when applied concurrently with BSO and DEM. The selective and cell-permeable H 2 S scavenger, SS20, inhibited the effects of LA on cellular H 2 S. Estimates of single-cell H 2 S production suggest that 0.1–0.2% of O 2 consumption is used to metabolize H 2 S and these requirements may increase to 1–2% with 1 mM LA. Collectively, these results suggest that LA rescues H 2 S from irreversible oxidation and that the effects of LA on RSS directly confer antioxidant, anti-inflammatory and cytoprotective responses. They also suggest that TS may be an effective supplement to increase the efficacy of LA in clinical settings. Protective effects of lipoic acid through rescue of reactive sulfur species (RSS). H 2 S derived from glutathione (GSH), cysteine (Cys) and protein catabolism is normally oxidized to sulfate (SO 4 2-) and excreted with thiosulfate (S 2 O 3 2-) as an intermediate in oxidation. Exogenous lipoic acid (LA) taken up by the cell is reduced to dihydrolipoic acid (DHLA) by thioredoxin (Trx), glutaredoxin (Grx) or peroxiredoxin (Prx) utilizing NADH as the reductant. DHLA reduces thiosulfate regenerating H 2 S which is then oxidized to persulfide (H 2 S 2), possibly by LA as the oxidant, although a catalyst for this reaction has not been identified. Persulfide is not only a strong antioxidant but it persulfidates regulatory cysteines that initiate a variety of transcriptional and post-transcriptional antioxidant, anti-inflammatory and cytoprotective defenses. Many of the "antioxidant" properties of LA can be explained by these RSS metabolic pathways. Image 1 [ABSTRACT FROM AUTHOR]

Life began in a ferruginous (anoxic and Fe2+ dominated) world around 3.8 billion years ago (bya). Hydrogen sulfide (H 2 S) and other sulfur molecules from hydrothermal vents and other fissures provided many key necessities for life's origin including catalytic platforms (primordial enzymes) that also served as primitive boundaries (cell walls), substrates for organic synthesis and a continuous source of energy in the form of reducing equivalents. Anoxigenic photosynthesis oxidizing H 2 S followed within a few hundred million years and laid the metabolic groundwork for oxidative photosynthesis some half-billion years later that slightly and episodically increased atmospheric oxygen around 2.3 bya. This oxidized terrestrial sulfur to sulfate which was washed to the sea where it was reduced creating vast euxinic (anoxic and sulfidic) areas. It was in this environment that eukaryotic cells appeared around 1.5 bya and where they evolved for nearly 1 billion additional years. Oxidative photosynthesis finally oxidized the oceans and around 0.6 bya oxygen levels in the atmosphere and oceans began to rise toward present day levels. This is purported to have been a life-threatening event due to the prevalence of reactive oxygen species (ROS) and thus necessitated the elaboration of chemical and enzymatic antioxidant mechanisms. However, these antioxidants initially appeared around the time of anoxigenic photosynthesis suggesting a commitment to metabolism of reactive sulfur species (RSS). This review examines these events and suggests that many of the biological attributes assigned to ROS may, in fact, be due to RSS. This is underscored by observations that ROS and RSS are chemically similar, often indistinguishable by analytical methods and the fact that the bulk of biochemical and physiological experiments are performed in unphysiologically oxic environments where ROS are artifactually favored over RSS. Image 1 • Sulfide (H 2 S) was key to the origin of life. • Nearly 80% of evolution occurred in sulfidic and hypoxic conditions. • Similarities between reactive sulfide species (RSS) and reactive oxygen species (ROS) blur the distinction between the two. • In extant organisms the significance of ROS may be over-estimated and the importance of RSS underappreciated. [ABSTRACT FROM AUTHOR]

Elaborate antioxidant pathways have evolved to minimize the threat of excessive reactive oxygen species (ROS) and to regulate ROS as signaling entities. ROS are chemically and functionally similar to reactive sulfur species (RSS) and both ROS and RSS have been shown to be metabolized by the antioxidant enzymes, superoxide dismutase and catalase. Here we use fluorophores to examine the effects of a variety of inhibitors of antioxidant pathways on metabolism of two important RSS, hydrogen sulfide (H 2 S with AzMC) and polysulfides (H 2 S n , where n = 2–7, with SSP4) in HEK293 cells. Cells were exposed to inhibitors for up to 5 days in normoxia (21% O 2) and hypoxia (5% O 2), conditions also known to affect ROS production. Decreasing intracellular glutathione (GSH) with l -buthionine-sulfoximine (BSO) or diethyl maleate (DEM) decreased H 2 S production for 5 days but did not affect H 2 S n. The glutathione reductase inhibitor, auranofin, initially decreased H 2 S and H 2 S n but after two days H 2 S n increased over controls. Inhibition of peroxiredoxins with conoidin A decreased H 2 S and increased H 2 S n , whereas the glutathione peroxidase inhibitor, tiopronin, increased H 2 S. Aminoadipic acid, an inhibitor of cystine uptake did not affect either H 2 S or H 2 S n. In buffer, the glutathione reductase and thioredoxin reductase inhibitor, 2-AAPA, the glutathione peroxidase mimetic, ebselen, and tiopronin variously reacted directly with AzMC and SSP4, reacted with H 2 S and H 2 S 2 , or optically interfered with AzMC or SSP4 fluorescence. Collectively these results show that antioxidant inhibitors, generally known for their ability to increase cellular ROS, have various effects on cellular RSS. These findings suggest that the inhibitors may affect cellular sulfur metabolism pathways that are not related to ROS production and in some instances they may directly affect RSS or the methods used to measure them. They also illustrate the importance of carefully evaluating RSS metabolism when biologically or pharmacologically attempting to manipulate ROS. Image 1 • Reactive oxygen species (ROS) and reactive sulfide species (RSS) are chemically and biologically similar. • Evolution of antioxidant pathways is more consistent with RSS metabolism than with ROS metabolism • Here we show that canonical inhibitors of ROS antioxidant pathways affect RSS in HEK293 cells independent of ROS. • These results indicate that antioxidant pathways are involved in RSS metabolism in cells. • RSS may be the actual effector pathway(s) of ROS antioxidant therapies. [ABSTRACT FROM AUTHOR]

The article offers information related to the floating villages on Tonle Sap Lake, Cambodia, and plans of China, Laos, and Cambodia to build dams for hydroelectricity and floodwater storage on the Mekong River upstream are viewed by environmentalists as threats to fisheries and riverbank farming.

It is now well established that hydrogen sulfide (H 2 S) is an effector of a wide variety of physiological processes. It is also clear that many of the effects of H 2 S are mediated through reactions with cysteine sulfur on regulatory proteins and most of these are not mediated directly by H 2 S but require prior oxidation of H 2 S and the formation of per- and polysulfides (H 2 S n , n = 2–8). Attendant with understanding the regulatory functions of H 2 S and H 2 S n is an appreciation of the mechanisms that control, i.e., both increase and decrease, their production and catabolism. Although a number of standard “conventional” pathways have been described and well characterized, novel “unconventional” pathways are continuously being identified. This review summarizes our current knowledge of both the conventional and unconventional. [ABSTRACT FROM AUTHOR]

The article discusses the construction of small dams by the Laotian government and proposed large dams on the Mekong main stem to meet energy needs for economic growth and increase export revenues.

Fluorescence spectroscopy and microscopy have been used extensively to monitor biomolecules, especially reactive oxygen species (ROS) and, more recently, reactive sulfide (RSS) species. Nearly all fluorophores are either excited by or emit light between 450 and 550 nm, which is similar to the absorbance of heme proteins and metal-centered porphyrins. Here we examined the effects of catalase (Cat), reduced and oxidized hemoglobin (Hb and metHb), albumin (alb), manganese (III) tetrakis (4-benzoic acid) porphyrin chloride (MnTBAP), iron protoporphyrin IX (hemin), and copper protoporphyrin IX (CuPPIX) on the fluorescence properties of fluorescein. We also examined the effects of catalase and MnTBAP on fluorophores for ROS (dichlorofluorescein, DCF), polysulfides (3=,6=-di(O-thiosalicyl)fluorescein, SSP4), and H2S (7-azido-4-methylcoumarin, AzMC) previously activated by H2O2, a mixed polysulfide (H2Sn, n = 1-7) and H2S, respectively. All except albumin concentration dependently inhibited fluorophore fluorescence and absorbed light between 450 and 550 nm, suggesting that the inhibitory effect was physical not catalytic. Catalase inhibition of fluorescein fluorescence was unaffected by sodium azide, dithiothreitol, diamide, tris(2-carboxyethyl)phosphine (TCEP), or iodoacetate, supporting a physical inhibitory mechanism. Catalase and TBAP augmented, then inhibited DCF fluorescence, but only inhibited SSP4 and AzMC fluorescence indicative of a substrate-specific catalytic oxidation of DCF and nonspecific fluorescence inhibition of all three fluorophores. These results suggest caution must be exercised when using any fluorescent tracers in the vicinity of metal-centered porphyrins. [ABSTRACT FROM AUTHOR]

The borders of Illinois were established when Illinois became a state in 1818. The western border was delineated using the Mississippi River, and the Ohio River was used as the southern border. The eastern border was formed by the Ohio and Wabash rivers as well as the line along the current longitude line of 87°31', connecting the Wabash River to Lake Michigan. As initially proposed, the northern border of Illinois would have been 51 miles to the south of the current latitude line of 42°30'30". This 5,440,000-acre addition to Illinois assured that the territory met the required minimum of 40,000 people to qualify as a state. [ABSTRACT FROM AUTHOR]

The article reports on the issues of managing the upper Missouri River for agriculture and irrigation and flood control, and energy and the effect of Ryan Dam and Garrison Dam on the river and the agriculture in the river valley and the human impacts of Garrison dam.

The article offers information on the sedimentation, navigation, and agriculture on the lower Missouri River at Saint Louis, Missouri; and also mentions the need of carving rocks and eroding soils to create channels and deepen through the continuous sediment transport and deposition processes.

The article discusses shift of soil functionality from optimal state to less optimal state based on water holding capacity as a function of soil organic carbon results soil degradation. Topics discussed include increase in runoff and sediment movements from agricultural landscapes due to increase in infiltration rate of soil; and increase in biodiversity reduce the vulnerability of ecosystem to tolerate adverse effects of climate change; and implication for crop management.

The article discusses the hundred year effort of the city of Chicago, Illinois to provide safe drinking water, which led to the establishment of the Illinois and Michigan canal, the investment to water treatment systems and the preservation of section of the Illinois and Michigan Canal at Lockport.

The article discusses the tons of sand dunes deposited at southern Illinois farmland and Dogtooth Bend peninsula which comes from the floodwaters of the Mississippi River in January of 2016, which required graders and snow plows to open the road for local traffic.

The article discusses the efforts of St. Johns Levee and Drainage District on the Mississippi River to mitigate internal flooding. The mitigation planning in the Bootheel of Missouri attempted to reduce the number of days communities are isolated by floodwaters, as well as to limit crop and non-crop losses and reduce damage through the adoption of strategies that reconnect the hydrology of the floodplain to the river. The changes in land use and drainage modifications over time are tackled.

The article discusses a study aimed to understand and highlight the effects of soil erosion, transport, and deposition on soil organic carbon (SOC) stock. Topics include soil erosion by wind and water and subsequent sediment transport and depositional processes to lead soil organic carbon (SOC) loss, soil management practices, basic types of agricultural land units type considerations when measuring SOC stock.

The article focuses on the intensive system of agriculture in Missouri bottomlands which results to good economic output and has altered the nutrient cycling, hydrology, and biodiversity of the entire ecosystem. It mentions that the Missouri's ecosystem is managed by the Little River Drainage District. A diagram is presented depicting the five drainage ditches in the southern Little River Drainage District.

The chemical versatility of sulfur and its abundance in the prebiotic Earth as reduced sulfide (H2S) implicate this molecule in the origin of life 3.8 billion years ago and also as a major source of energy in the first seven-eighths of evolution. The tremendous increase in ambient oxygen ~600 million years ago brought an end to H2S as an energy source, and H2S-dependent animals either became extinct, retreated to isolated sulfide niches, or adapted. The first 3 billion years of molecular tinkering were not lost, however, and much of this biochemical armamentarium easily adapted to an oxic environment where it contributes to metabolism and signaling even in humans. This review examines the role of H2S in evolution and the evolution of H2S metabolism and signaling. [ABSTRACT FROM AUTHOR]

The article discusses the construction of the Headwaters Diversion channel to help drain and protect 480,000 ha of agricultural lands in southeast Missouri from internal seasonal flooding and Mississippi River backflow at flood stage. Central to this success was the diversion of water coming from the Ozark Plateau and Francois Mountains directly into the Mississippi River using a series of leveed channels in order to isolate the upper basin and prevent overloading of the lower drainage system.

The article focuses on the installation of slurry trenches and relief wells to strengthen Ohio and Mississippi river levee systems. Topics discussed include historical geological features of the Cache River valley area, consequences of cache river levee failure in Ohio and Mississippi, restoration of cache river levees, impact of flooding on farmland located North of Cairo area, and impact of 2011 flooding on unleveed agricultural lands.

The article focuses on the development and repair of sinkholes and sand boils after flood of 2011 in Cairo, Illinois. Topics discussed include emergence of sinkholes and sand boils, treatment of roads by the U.S. Army Corps of Engineers (USACE), lack of crop insurance benefits to farmers for crop damage, soil erosion caused because of failure of levees, and vegetation on the Angelo Towhead island.

Significance: Although oxygen (O2)-sensing cells and tissues have been known for decades, the identity of the O2-sensing mechanism has remained elusive. Evidence is accumulating that O2-dependent metabolism of hydrogen sulfide (H2S) is this enigmatic O2 sensor. Recent Advances: The elucidation of biochemical pathways involved in H2S synthesis and metabolism have shown that reciprocal H2S/O2 interactions have been inexorably linked throughout eukaryotic evolution; there are multiple foci by which O2 controls H2S inactivation, and the effects of H2S on downstream signaling events are consistent with those activated by hypoxia. H2S-mediated O2 sensing has been demonstrated in a variety of O2-sensing tissues in vertebrate cardiovascular and respiratory systems, including smooth muscle in systemic and respiratory blood vessels and airways, carotid body, adrenal medulla, and other peripheral as well as central chemoreceptors. Critical Issues: Information is now needed on the intracellular location and stoichometry of these signaling processes and how and which downstream effectors are activated by H2S and its metabolites. Future Directions: Development of specific inhibitors of H2S metabolism and effector activation as well as cellular organelle-targeted compounds that release H2S in a time- or environmentally controlled way will not only enhance our understanding of this signaling process but also provide direction for future therapeutic applications. Antioxid. Redox Signal. 22, 377-397. [ABSTRACT FROM AUTHOR]

The article reviews the paired comparison approach used by many scientists to determine soil carbon sequestration rates and discusses the questions raised by this approach on the validity of the results of soil organic carbon (SOC) sequestration estimation. A review of available literature indicates that the difference between the no-tillage (NT) and conventional tillage (CT) treatments at the end of a long-term study using a paired plot approach is just a measure of net SOC storage difference.

Hydrogen sulfide (H 2 S) signaling has been implicated in physiological processes in practically all organ systems studied to date. At times the excitement of this new field has outpaced the technical expertise or practical knowledge with which to accurately assess these advancements. Recently, the myriad of proposed H 2 S actions has spawned interest in using indicators of H 2 S metabolism, especially plasma H 2 S concentrations, as a means of identifying a variety of pathophysiological conditions or to predict clinical outcomes. While this is a noteworthy endeavor, there are a number of contraindications to this practice at this time. First, there is little consensus regarding normal, i.e., “physiological” concentrations of H 2 S in either plasma or tissue. In fact, it has been shown that the methods most often employed for these measurements are associated with substantial artifact. Second, interactions, or presumed lack thereof, of H 2 S with other biomolecules (e.g., O 2 , H 2 O 2 , pH, etc.) or analytical reagents (e.g., reducing reagents, N -ethylmaleimide, phenylarsine, etc.) are often assumed but not evaluated. Third, the experimental design and/or statistical analyses may not be sufficient to justify using H 2 S concentration in tissue or blood as a predictive biomarker of pathophysiology. In this study, we first briefly review the problems associated with plasma and tissue H 2 S measurements and the associated errors and we provide some simple methods to evaluate whether the data obtained is physiologically relevant. Second we provide a brief analysis of H 2 S interactions with the above biomolecules. Third, we provide a statistical tool with which to determine the clinical applicability of H 2 S measurements. It is hoped that these points will provide a rational background for future work. [ABSTRACT FROM AUTHOR]

The article discusses the barges accident that damaged the Marseilles Lock and Dam during 2013 flood on the Illinois River. Topics mentioned include the documenting of the damages to the dam structure, the construction of the Illinois waterway system and the Marseilles lock and dam system designed by the U.S. Army Corps of Engineers (USACE) as a unit in maintaining the shipping channel and other types of water traffic.

In agricultural land areas, no-tillage (NT) farming systems have been practiced to replace intensive tillage practices such as, moldboard plow (MP), chisel plow (CP), and other systems to improve many soil health indicators, and specifically to increase soil organic carbon (SOC) sequestration and reduce soil erosion. Numerous approaches to estimate the amounts and rates of SOC sequestration as a result of a switch to NT systems have been published, but there is a concern regarding protocol for assessing SOC especially for different tillage systems. Therefore, the objectives of this paper are to: (i) define and understand concepts of SOC sequestration, (ii) quantify SOC distribution and the methodology of measurements, (iii) address soil spatial variability at field- or landscape-scale for potential SOC sequestration, and (iv) consider proper field experimental design, including pretreatments baseline for SOC sequestration determination. For SOC sequestration to occur, as a result of a treatment applied to a land unit, all of the SOC sequestered must originate from the atmospheric CO2 pool and be transferred into the soil humus through land unit plants, plant residues, and other organic solids. The SOC stock present in soil humus at end of a study must be greater than the pretreatment SOC stock levels in the same land unit. However, one should recognize that a continuity equation showing drawdown in atmospheric concentration of CO2 may be difficult, if not impossible, to quantify. Therefore, SOC sequestration results of paired comparisons of NT to other conventional tillage systems with no pretreatments SOC baseline, and if the conventional system is not at a steady state, will likely be inaccurate where the potential for SOC loss exists in both systems. To unequivocally demonstrate that the SOC sequestration has occurred at a specific site, a temporal increase must be documented relative to pretreatment SOC content and linked attendant changes in soil properties and ecosystem services and functions with proper consideration given to soil spatial variability. Also, a standardized methodology that includes proper experimental design, pretreatment baseline, root zone soil depth consideration, and consistent method of SOC analysis must be used when determining SOC sequestration. [ABSTRACT FROM AUTHOR]

The article focuses on drought conditions in the Mississippi River Channel at Thebes, Illinois as a result of slow soaking rain systems and evening thunder-storms. Topics discussed include a new challenge for the U.S. Army Corps of Engineers (USACE) to control the Mississippi River, lack of rain throughout 2012 that severe summertime seasonal drought over the central Great Plains and USACE's successful effort to dredge other parts of the Mississippi River to keep the shipping channel open.

The article offers information on the flooding of the Ohio River at the Cache River Valley in south Illinois in the later part of April ad early part of May in 2011. It mentions that the flood is caused by the early snowmelt and heavy rains at the eastern part of Ohio Basin and it resulted to the rise of Ohio River's gage to 18.7 meters. Moreover, the counties affected by the flood and the geological attributes of the Cache River Valley are also stated.

H2S derived from organic thiol metabolism has been proposed serve as an oxygen sensor in a variety of systems because of its susceptibility to oxidation and its ability to mimic hypoxic responses in numerous oxygen-sensing tissues. Thiosulfate, an intermediate in oxidative H2S metabolism can alternatively be reduced and regenerate H2S. We propose that this contributes to the H2S-mediated oxygen-sensing mechanism. H2S formation from thiosulfate in buffers and in a variety of mammalian tissues and in lamprey dorsal aorta was examined in real time using a polarographic H2S sensor. Inferences of intracellular H2S production were made by examining hypoxic pulmonary vasoconstriction (HPV) in bovine pulmonary arteries under conditions in which increased H2S production would be expected and in mouse and rat aortas, where reducing conditions should mediate vasorelaxation. In Krebs-Henseleit (mammalian) and Cortland (lamprey) buffers, H2S was generated from thiosulfate in the presence of the exogenous reducing agent, DTT, or the endogenous reductant dihydrolipoic acid (DHLA). Both the magnitude and rate of H2S production were greatly increased by these reductants in the presence of tissue, with the most notable effects occurring in the liver. H2S production was only observed when tissues were hypoxic; exposure to room air, or injecting oxygen inhibited H2S production and resulted in net H2S consumption. Both DTT and DHLA augmented HPV, and DHLA dosedependently relaxed precontracted mouse and rat aortas. These results indicate that thiosulfate can contribute to H2S signaling under hypoxic conditions and that this is not only a ready source of H2S production but also serves as a means of recycling sulfur and thereby conserving biologically relevant thiols. [ABSTRACT FROM AUTHOR]

This invited Editorial addresses the rescue of the article by Xue et al. "Hydrogen sulfide treatment promotes glucose uptake by increasing insulin receptor sensitivity and ameliorates kidney lesions in type 2 diabetes.'' The work was rejected by the standard peer review system and subsequently rescued via the Rebound Peer Review mechanism offered by Antioxidants and Redox Signaling (Antoxid Redox Signal 16: 293-296, 2012). The open reviewers rescuing the work were Jin-Song Bian, Samuel Dudley, Hideo Kimura, and Xian Wang. The initial article was reviewed by six reviewers who had valid concerns; they recommended extensive revision and additional experiments. In the subsequent two iterations, the authors nearly doubled the number of experiments and made substantial revisions. However, several reviewers were still not satisfied, and the authors requested the rebound pathway. The open reviewers, selected by the authors and experts in hydrogen sulfide biology, diabetes, and cardiovascular physiology, added a broad perspective to the review process. They acknowledged the anonymous reviewer's concerns, but felt that the merits of the study were sufficient to recommend acceptance. The open reviewers also identified several situations where the recommendations of the anonymous reviewers and the author's attempts to rectify them were moot, given the available methodology and present state of the field. From this perspective, the rebound track was a success; it rescued an article that otherwise would have been rejected and will stimulate further discussion and research in this area. Whether or not there are more efficient ways to accomplish, this remains to be determined. [ABSTRACT FROM AUTHOR]

The article focuses on the failure of the Len Small levee during the Ohio River Flood of 2011 in Illinois. It discusses the architectural features of the extensive systems of the U.S. Army Corps of Engineers (USACE) and private levees that confine the Mississippi River and protect the low-lying agricultural lands, rural towns, and public conservation areas from flooding. The Small Len levee built on the southern Illinois border near Cairo protects private and public lands from 20-year floods.

Abstract: Hydrogen sulfide (H2S) metabolism has been proposed as the oxygen (O2) sensing mechanism coupling hypoxia to effector responses in a variety of tissues including vascular and chemoreceptor cells. Implicit in this sensing system is a mechanism for regulating intracellular H2S concentration, presumably through oxidation. However, verification of this mechanism, or any other pathway of H2S signaling has been hampered by the lack of suitable methods for measuring intracellular concentration and distribution profiles. Here, intracellular H2S concentration profiles are modeled using simple monoexponential diffusion equations and current knowledge of H2S biosynthetic and metabolic pathways. The models predict that; (1) while both mitochondrial oxidation and simple diffusion out of the cell can reduce H2S concentration, the former is considerably more effective as an effector of intracellular H2S and (2) exogenously applied H2S may have unanticipated effects on endogenous signaling processes. In addition, these models provide additional support for mitochondrial H2S oxidation as the key couple in H2S-mediated O2 sensing. [Copyright &y& Elsevier]

Abstract: The atmospheric levels of carbon dioxide (CO2) have been due largely to the burning of fossil fuels, deforestation, cultivation of the grasslands, drainage of the land, and land use changes. This has led to increase in greenhouse gases, created concerns about the potential for long-term climate change and interest in developing methods to sequester some of this atmospheric carbon. In agricultural land areas no-tillage (NT) systems have been proposed, to replace moldboard plow and chisel systems as a way to sequester soil organic carbon (SOC). Numerous estimates have been published of soil organic carbon (SOC) sequestration total and rates as a result of a switch to NT systems. Other researchers have proposed the use of cover crops, synthetic fertilizers, organic fertilizer, manure, liming, agricultural systems and management, agroforestry, forages, compost, crop rotations, and reduced row crop use as ways to sequester SOC. For SOC sequestration to occur as a result of a treatment applied to a land unit, all of the SOC sequestered must have come from atmosphere and be transferred into the soil humus through the unit plants, plant residues and other organic solids. The amount of SOC present in the soil humus at the end of the study has to be greater than the pre-treatment SOC levels in the same land unit and there needs to be a net depletion of atmospheric CO2 as a result. The objectives of this paper are to: (1) determine long-term study SOC levels and trends in agricultural lands, (2) application of the SOC sequestration concept to a specific site, (3) identify appropriate experimental designs for plot area use in determining SOC sequestration, (4) develop a procedure, such as pre-treatment measurements of SOC levels in the plots before treatments are applied, to verify SOC sequestration at a site (5) equivalent soil mass sampling method, (6) compare laboratory methods for quantifying SOC content, and (7) account for the loading of C rich amendments. To unequivocally demonstrate SOC sequestration at a specific site has occurred, a temporal increase must be documented relative to pre-treatment SOC level and linked to a net depletion of atmospheric CO2. [Copyright &y& Elsevier]

Abstract: Hydrogen sulfide, H2S, is a colorless gas with a strong odor that until recently was only considered to be a toxic environmental pollutant with little or no physiological significance. However, the past few years have demonstrated its role in many biological systems and it is becoming increasingly clear that H2S is likely to join nitric oxide (NO) and carbon monoxide (CO) as a major player in mammalian biology. In this review, we have provided an overview of the chemistry and biology of H2S and have summarized the chemistry and biological activity of some natural and synthetic H2S-donating compounds. The naturally occurring compounds discussed include, garlic, sulforaphane, erucin, and iberin. The synthetic H2S donors reviewed include, GYY4137; cysteine analogs; S-propyl cysteine, S-allyl cysteine, S-propargyl cysteine, and N-acetyl cysteine. Dithiolethione and its NSAID and other chimeras such as, L-DOPA, sildenafil, aspirin, diclofenac, naproxen, ibuprofen, indomethacin, and mesalamine have also been reviewed in detail. The newly reported NOSH-aspirin that releases both NO and H2S has also been discussed. [Copyright &y& Elsevier]

In this article, the authors discuss the breaching of levees in the New Madrid Floodway, Missouri in May 2011. They explain that changing climate conditions will intensify the risks regarding snow melting, rain fall and flooding. They suggest that a comprehensive plan which promotes the leveed engineering infrastructure with redevelopment of an ecological infrastructure can lessen flooding and strengthen the effectiveness of well placed leveed systems.

The ability to monitor oxygen (O2) availability and delivery is crucial to an animal's survival. Vertebrates have a number of O2 'sensing' cells that monitor environmental oxygen and ensure adequate delivery to the tissues. While there is little doubt that these cells perform important homeostatic functions, there is little consensus on how a change in O2 concentration, or partial pressure (pO2), is transduced into a physiological response. We recently proposed that the metabolism of hydrogen sulfide (H2S) functions as the O2 sensor in a variety of tissues. In this mechanism, the concentration of biologically active H2S is regulated by the simple balance between constitutive H2S production and its oxidation by mitochondria. This hypothesis is supported by a number of experimental observations in a wide range of O2 sensing tissues: 1) exogenous H2S produces the same physiological response as hypoxia; 2) cellular H2S production is inversely related to pO2 at physiologically relevant pO2s; 3) agonists and antagonists of H2S biosynthesis augment and inhibit hypoxic responses, respectively; and 4) H2S and hypoxia appear to act via common effector pathways. The reciprocal relationship between H2S and O2 also has a long evolutionary history suggesting these gases have been inexorably intertwined throughout evolution. The intent of this review is to elaborate on the mechanism of H2S-mediated O2 sensing. [ABSTRACT FROM AUTHOR]

The article presents information on the restoration of the land that were destroyed during the flood in 2011 in the U.S. It informs that the 100 hectare of land was converted into deep gullies and eroded tons of soil, damaging irrigation equipment, farm buildings and homes. It further informs that the reclamation and restoration of these lands very time consuming.

Abstract: The concept that non-respiratory gases, such as nitric oxide (NO), carbon monoxide (CO) and hydrogen sulfide (H2S) functioned as signaling moieties is a relatively recent development, due in part to their ephemeral existence in biological tissues. However, from an evolutionary perspective these gases dominated the prebiotic and anoxic Earth and were major contributors to the origin of life and the advent of eukaryotic animals. As Earth''s oxygen levels rose, NO, CO and H2S disappeared from the environment and cells began to utilize their now well-developed metabolic pathways to compartmentalize and regulate these three gases for signaling purposes. Ironically, many of the signaling pathways have become now intimately involved in regulating oxygen delivery and their evolution has continued well into the vertebrates. This review examines the role NO, CO and H2S played in early life and their regulatory roles in oxygen delivery during the course of vertebrate evolution. [Copyright &y& Elsevier]

Hypoxic pulmonary vasoconstriction (HPV) is an adaptive response that diverts pulmonary blood flow from poorly ventilated and hypoxic areas of the lung to more well-ventilated parts. This response is important for the local matching of blood perfusion to ventilation and improves pulmonary gas exchange efficiency. HPV is an ancient and highly conserved response, expressed in the respiratory organs of all vertebrates, including lungs of mammals, birds, and reptiles; amphibian skin; and fish gills. The mechanism underlying HPV and how cells sense low PO2 remains elusive. In perfused trout gills (Oncorhynchus mykiss), acute hypoxia, as well as H2S, caused an initial and transient constriction of the vasculature. Inhibition of the enzymes cystathionine- γ-synthase and cystathionine-γ-lyase, which blocks H2S production, abolished the hypoxic response. Individually blocking the four complexes in the electron transport chain abolished both the hypoxic and the H2S-mediated constriction. Glutathione, an antioxidant and scavenger of superoxide, attenuated the vasoconstriction in response to hypoxia and H2S. Furthermore, diethyldithiocarbamate, an inhibitor of superoxide dismutase, attenuated the hypoxic and H2S constriction. This strongly suggests that H2S mediates the hypoxic vasoconstriction in trout gills. H2S may stimulate the mitochondrial production of superoxide, which is then converted to hydrogen peroxide (H2O2). Thus, H2O2 may act as the "downstream" signaling molecule in hypoxic vasoconstriction. [ABSTRACT FROM AUTHOR]

The article focuses on the effects of the flooding in Cairo, Illinois, which was caused by the swelling of the Mississippi and Ohio rivers in 2011. It says that Cairo is situated at the confluence of the two rivers, wherein the Fort Defiance State Park was under water in the April 2011 flooding, as well as the Illinois farmlands. Furthermore, the decision of the U.S. Army Corps of Engineers (USACE) to blow up the New Madrid Floodway helped to lessen the impact of the flood.

The article discusses the impact of 2011 induced levee breaches on agricultural lands in Mississippi River Valley. It mentions that the breaching was a planned strategy to reduce water pressure and prevent levee failures. It states that the New Madrid Floodway project in the river was designed by the U.S. Army Corps of Engineers (USACE), which obtained modified flowage easements within the Floodway lands to permit the expected artificial breaching.

Abstract: There is considerable controversy surrounding the initial step that transduces a fall in into a physiological signal, i.e., the “oxygen sensor” in chemoreceptors. Initial studies on systemic and respiratory vessels suggested that the metabolism of hydrogen sulfide (H2S) could serve as the oxygen sensor. This model was subsequently extended to chemoreceptors in fish and tissues of other animals. In this model, constitutive production of biologically active H2S is offset by H2S oxidation; when oxygen availability falls, production of H2S exceeds metabolism, and the resultant increase in intracellular H2S initiates the appropriate physiological responses. This model is supported by observations that the effects of hypoxia and H2S are similar, if not identical in many tissues: hypoxic responses are inhibited by inhibitors of H2S biosynthesis and augmented by sulfur donating molecules, and the tipping point between H2S production and oxidation occurs at physiologically relevant . Recent studies from other laboratories support this mechanism of O2 sensing in the carotid body. This review summarizes information that supports the H2S metabolic hypothesis in these tissues with emphasis on the carotid chemoreceptors. Evidence suggesting that H2S is not involved in oxygen sensing in the carotid body is also critically evaluated. [Copyright &y& Elsevier]

Hydrogen sulfide (H2S) has become the hot new signaling molecule that seemingly affects all organ systems and biological processes in which it has been investigated. It has also been shown to have both proinflammatory and anti-inflammatory actions and proapoptotic and anti-apoptotic effects and has even been reported to induce a hypometabolic state (suspended animation) in a few vertebrates. The exuberance over potential clinical applications of natural and synthetic H2S-"donating" compounds is understandable and a number of these function-targeted drugs have been developed and show clinical promise. However, the concentration of H2S in tissues and blood, as well as the intrinsic factors that affect these levels, has not been resolved, and it is imperative to address these points to distinguish between the physiological, pharmacological, and toxicological effects of this molecule. This review will provide an overview of H2S metabolism, a summary of many of its reported "physiological" actions, and it will discuss the recent development of a number of H2S-donating drugs that show clinical potential. It will also examine some of the misconceptions of H2S chemistry that have appeared in the literature and attempt to realign the definition of "physiological" H2S concentrations upon which much of this exuberance has been established. [ABSTRACT FROM AUTHOR]