What Is Oxygen's Role In Cellular Respiration – , abundant ROS is important in many ways, or otherwise. ROS act as signals that turn biological functions on and off. They are intermediates in the O redox process

, ctral to fuel cells. ROS are critical to the photodegradation of organic pollutants in the atmosphere. For the most part, ROS are considered in a biological context, from their effects on aging and their role in causing dangerous genetic mutations.

What Is Oxygen's Role In Cellular Respiration

ROS are not uniformly defined. All sources include superoxide, singlet oxygen and hydroxyl radical. Hydrogen peroxide is not as reactive as these species, but it is activated very quickly and thus absorbed.

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Competing with its formation, superoxide is destroyed by superoxide dismutases, enzymes that catalyze its disproportionation:

In a biological context, ROS are products of normal oxygen metabolism. ROS play a role in cell signaling and homeostasis.

In plants, ROS are involved in metabolic processes related to photoprotection and tolerance to various stresses.

However, ROS can cause irreversible damage to DNA because they oxidize and modify cellular components and prevent them from performing their basic functions. This suggests that ROS plays a dual role; whether they act as deleterious, protective or signaling factors, producing ROS and disposing of them when and where they are needed.

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In other words, oxygen toxicity can arise from both uncontrolled production and ineffective removal of ROS by the antioxidant system. During environmental stress (eg, UV or heat exposure), ROS levels can increase dramatically.

This can cause significant damage to cell structures. Collectively, this is called oxidative stress. ROS production is strongly influenced by the stress response in plants, and factors that increase ROS production include drought, salinity, chilling, pathogen extinction, nutrient deficiency, metal toxicity, and UV-B radiation. ROS are also regenerated by exogenous sources such as ionizing radiation

ROS are produced during the processes of respiration and photosynthesis in organelles such as mitochondria, peroxisomes and chloroplasts.

During respiration, mitochondria convert energy into a usable form for the cell, adenosine triphosphate (ATP). The process of producing ATP in mitochondria, called oxidative phosphorylation, involves the transport of protons (hydrogen ions) across the inner mitochondrial membrane via the electron transport chain. In the electron transport chain, electrons pass through a series of redox reactions through a series of proteins, with each accessory protein further down the chain being reduced to a greater degree than the previous one. The final destination for an electron along this chain is the oxygen molecule. Under normal conditions, oxygen is reduced to produce water; however, in about 0.2% of the electrons passing through the chain (this number comes from studies of isolated mitochondria, the exact rate in living organisms has yet to be fully agreed upon), oxygen is prematurely and completely reduced instead. superoxide radical (

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Another source of ROS production in animal cells is electron transfer reactions catalyzed by mitochondrial P450 systems in steroidogenic tissues.

These P450 systems are used to transfer electrons from NADPH to P450. During this process, some electrons “leak out” and react with O

Superoxide production. To combat this natural source of ROS, steroidogenic tissues, ovaries and testes, have high concentrations of antioxidants such as vitamin C (ascorbate) and β-carotene and antioxidant enzymes.

In addition, ROS are produced in immune cell signaling through the NOX pathway. Phagocytic cells such as neutrophils, eosinophils and mononuclear phagocytes produce stimulated ROS.

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Carboxylation and oxidation reactions in chloroplasts are catalyzed by Rubisco, and the electron transport chain (ETC) is believed to function in an O-rich environment.

The ETC in the photosystem (PSI) was once thought to be the sole source of ROS in chloroplasts. The flow of electrons from the catalyzed reaction catalyzes NADP and is reduced to NADPH, which enters the Calvin cycle and reduces the final electron acceptor, CO

When the ETC is overloaded, part of the electron flow is diverted from ferredoxin to O

PSI can be from 2Fe-2S and 4Fe-4S clusters in ETC. However, PSII also provides electron-draining sites (QA, QB) for O

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) bound to PSII instead of PSI; QB is shown as the origin of O

Tobacco, smoke, drugs, hobbies, microplastics or radiation. In plants, in addition to exposure to abiotic factors, high temperatures and interactions with other organisms can affect ROS production.

Ionizing radiation can cause harmful intermediates to interact with water, a process called radiolysis. Since water makes up 55-60% of the human body, the probability of radiolysis under ionizing radiation is quite high. In this process, water loses an electron and becomes very reactive. Through a three-step chain reaction, water is converted to a hydroxyl radical (

The hydroxyl radical is highly reactive and immediately removes an electron from any molecule in its path, turning that molecule into a free radical and thus propagating a chain reaction. However, hydrogen peroxide is more damaging to DNA than hydroxyl radicals because the lower reactivity of hydrogen peroxide allows more time for the molecule to enter the cell nucleus and react with macromolecules such as DNA.

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The production of ROS in plants leads to a reduction or disruption of metabolic activity during abiotic stress. For example, increasing temperature and drought are limiting factors for CO availability

Can lead to reprogramming of nuclear gene expression leading to chlorosis and programmed cell death in chloroplasts.

In case of biotic stress, the generation of ROS becomes rapid and weak and becomes more intense and persistent.

The first phase of ROS accumulation is associated with plant infection and probably involves the synthesis of new ROS-induced hematological enzymes. However, a second phase of ROS accumulation is associated with infection with non-viral pathogens and increases mRNA transcription encoding enzymes.

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Superoxide dismutases (SOD) are a class of enzymes that catalyze the breakdown of superoxide into oxygen and hydrogen peroxide. Thus, they are an important antioxidant deficiency in almost all cells exposed to oxygen. In mammals and most chordates, three forms of superoxide dismutase are perst. SOD1 is primarily in the cytoplasm, SOD2 in mitochondria and SOD3 extracellularly. The first is a dimer (consisting of two subunits) and the others are tetramers (four subunits). SOD1 and SOD3 contain copper and zinc ions, while SOD2 has a manganese ion in its reactive region. Ges is located on chromosomes 21, 6, and 4 (21q22.1, 6q25.3, and 4p15.3-p15.1).

Where M = Cu (n = 1); Mn (n = 2); Fe (n = 2); Ni (n = 2). In this reaction, the oxidation state of the metal cation ends up in the n and n + 1 vibrations.

Catalase, concentrated in peroxisomes located near mitochondria, reacts with hydrogen peroxide to catalyze the formation of water and oxygen. Glutathione peroxide reduces hydrogen peroxide by transferring the energy of reactive peroxides to a sulfur-containing tripeptide called glutathione. The sulfur in these enzymes acts as a reactive cation, transferring reactive electrons from peroxide to glutathione. Peroxiredoxins are also degraded

2 H 2 O 2 → catalase 2 H 2 O + O 2 2 GSH + H 2 O 2 → glutathione peroxidase GS – SG + 2 H 2 O & 2H2O + O2}} \ & + H2O2 -> [] [} atop GS-SG + 2H2O}}d}}

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Free radical mechanisms in genetic injury. Free radical detoxification induced by probiotics and subsecute detoxification by cellular enzymes.

These include not only roles in apoptosis (programmed cell death), but also positive effects such as induction of host defects.

It controls them with mobile functionality. In particular, platelets involved in wound repair and blood homeostasis release ROS to recruit additional platelets to sites of injury. They also link to the adaptive immune system through the recruitment of leukocytes.

Reactive oxygen species affect cellular function in a variety of inflammatory responses, including cardiovascular disease. They can also cause hearing loss from increased noise levels, ototoxicity of drugs such as cisplatin, and deafness in both animals and humans.

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ROS are also involved in mediating apoptosis or programmed cell death and ischemic injury. Specific examples include stroke and heart attack.

In general, the cellular effects of reactive oxygen species include damage to DNA or RNA, oxidation of polyunsaturated fatty acids in lipids (lipid peroxidation), oxidation of amino acids in proteins, and oxidative deactivation of specific enzymes. factors.

When a plant recognizes an invading pathogen, one of the first reactions is the rapid production of superoxide (O− 2 ) or hydrogen peroxide (H 2 O 2 ) to strengthen the cell wall. This prevents the pathogen from spreading to other parts of the plant, forming a net around the pathogen to limit movement and reproduction.

To illustrate the importance of these deficits, people with chronic granulomatous disease who have deficits in ROS scavenging are susceptible.

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