OBVS’s Nikam College of Pharmacy, Gondur, Dhule
Review article base on Free radicals are highly reactive and unstable molecules. Some of the key free radicals include hydroxyl radical, superoxide anion, hydrogen peroxide, singlet oxygen, hypochlorite, nitric oxide, and peroxynitrite. These radicals can damage important biological molecules like DNA, proteins, carbohydrates, and lipids, leading to cell damage. They are also linked to problems like early aging. Both internal and external factors can trigger the production of these reactive species, and oxidative stress plays a major role in many inflammatory diseases. Antioxidants can help neutralize the harmful effects of free radicals. They act by scavenging radicals, donating hydrogen or electrons, breaking down peroxides, quenching singlet oxygen, inhibiting enzymes, working synergistically, and chelating metals. Many natural antioxidants are available, including vitamins (like Vitamin C and E) and enzymes (such as glutathione reductase, glutathione peroxidases, and superoxide dismutase).
A free radical is any molecular species that contains an unpaired electron in its atomic orbital. This unpaired electron gives free radicals their typical properties, making many of them unstable and highly reactive. They can either donate or accept electrons from other molecules, functioning as oxidizing or reducing agents.
The most significant oxygen-containing free radicals involved in various disease conditions include hydroxyl radicals, superoxide anion radicals, hydrogen peroxide, singlet oxygen, hypochlorite, nitric oxide radicals, and peroxynitrite radicals. These highly reactive species can damage crucial biological molecules such as DNA, proteins, carbohydrates, and lipids. By attacking these macromolecules, free radicals cause cellular damage and disrupt the body's balance, or homeostasis.
In the body, free radicals can target a wide range of molecules, with lipids, nucleic acids, and proteins being the primary targets.
Generation of reactive oxygen species in the human body:
Free radicals and other reactive oxygen species (ROS) arise from normal basic metabolic processes in the body or from external sources such as exposure to x-rays, ozone, cigarette smoking, air pollutants, and industrial chemicals.
Figure 1: Generation of reactive oxygen species in the human body.
Free radicals are formed as a result, they are continuously in the cells as a consequence of bothEnzymatically and non-enzymatically
Figure 2: Generation of free radical and ROS.
Some internal sources of free radicals:
Some external sources of free radicals:
Ozone can be harmful or beneficial, depending on where it is found. In the troposphere, ozone is called smog. This particular type can be formed by free radicals.However, ozone acts as a shield in the stratosphere. Ozone completely protects the Earth's surface from UV-C radiation. Some UV-.B (which causes more sunburn) and UV- A (which causes more tanning) still reach the Earth's environment.
Figure 3: Ozone completely protects the Earth's surface from UV-C radiation.
Free Radicals in Biology
Free radical reactions are expected to cause progressive adverse effects that accumulate throughout the body as we age.
Figure 4: Free Radicals in Biology.
Depending on genetic and environmental factors, they manifest as diseases at a certain age.Cancer and atherosclerosis, the two leading causes of death, are prominent "free radical" diseases. The initiation and development of cancer is associated with chromosomal defects and the activation of oncogenes.
Antioxidants :
Antioxidants are molecules that are stable enough to donate electrons to vicious free radicals and neutralize them, thereby reducing their ability to cause damage. These antioxidants primarily delay or inhibit cellular damage through their ability to scavenge free radicals.
Figure 5: Effect of Antioxidants on free radicals.
These small molecule antioxidants can safely interactwith reactive oxygen speciesand haltthe chain reaction before important molecules are damaged.
The concept of oxidative stress:
The term is used to describe a state of oxidative damage resulting from an unfavorable critical balance between free radical production and antioxidant defenses. A role for oxidative stress has been postulated in many conditions, includingatherosclerosis, inflammatory diseases, some cancers, and the aging process. Oxidative stress is now thought to be a significant cause of all inflammatory diseases (arthritis, vasculitis, glomerulonephritis, lupus erythematosus, adult respiratory distress syndrome), ischemic diseases (heart disease, stroke, intestinal ischemia), hemochromatosis, AIDS, emphysema, organ transplantation, peptic ulcers, hypertension and preeclampsia, neurological diseases (Alzheimer's disease, Parkinson's disease, muscular dystrophy), alcoholism, and smoking-related diseases. Excessive oxidative stress can lead to oxidation of lipids and proteins, which is associated with changes in their structure and function.
Free Radical Creating Complications:
Vitamin C may help prevent cancer. Possible mechanisms by which vitamin C may affect carcinogenesis include antioxidant effects, blocking nitrosamine production, enhancing immune responses, and accelerating liver detoxification enzymes. Vitamin E, an important antioxidant, plays a critical role in immune function by enhancing humoral antibody defense, resistance to bacterial infection, cellular immunity, T cell tumor necrosis factor production, inhibition of mutagenic agent formation, DNA membrane repair, and blocking microglial lineage formation.
Figure 8: The primary mechanism of aging involves the accumulation of DNA or cellular and functional damage.
Figure 9: Effect of antioxidant on human body.
Oxidative damage to protein products can affect enzyme activity, receptors, and membrane transport. Protein oxidation causes aging by affecting signaling mechanisms, enzyme activity, thermal stability, and changes in susceptibility to protein degradation
Antioxidant Defense System:
Levels of antioxidant action:
Enzymatic:
Non-Enzymatic:
Superoxide dismutase:
Catalase:
Glutathione systems:
Nutraceutical:
CONCLUSION
As various studies suggest that these free radicles are very harmful for body and they play very vital role in the pathogenesis of various diseases like cancer, cardiovascular diseases, cellular and DNA damage, aging etc. This oxidative damage to the cellsis permanent which cannot be reversed. There are many sources for the generation of these free radicles. The action of these free radicles depends upon their ability to donate electrons to other chemical groups thereby initiating the chain reactions. These chain reactions can be arrest by use of antioxidants and further damage can be prevented. Some naturally occurring antioxidants can prove effective like Vit. C, Vit. E, Catalase, Superoxide dismutase etc. Whereas the synthetic antioxidants can produce harmful side effects on body. Person should consume the bright colored food which provides a natural antioxidants like vegetables, fruits etc. These substances contain phenolic compounds which are considered as very potent antioxidants.
ACKNOWLEDGMENT
Deepest gratitude is also extended to Professor Ravindra Nikam and the College of Pharmacy in Gondur, Dhule, for kindly providing essential research facilities. Furthermore, I would like to convey my thanks to Dr. A. V. Patil, the Principal of Prof. Ravindra Nikam College of Pharmacy in Gondur and Dhule, for their consistent encouragement and support throughout this make an effort.
Conflict of Interest:
The writer affirms that there are no conflicts of interest to disclose.
Ethical Approval:
Not applicable.
Funding:
Not applicable.
Declarations:
I state that any work of others used in this paper has been appropriately cited and attributed. Any
Assistance received in the research, writing, or editing of this paper has been duly acknowledged.
REFERENCES
Lokesh A. Gurav, Kishan A. Zodage, Amit P. Sinhal, Atish A. Salunkhe, Jitendra D. More, Exploring the Potential of Antioxidants in Reducing Free Radicals: A Comprehensive Review, Int. J. of Pharm. Sci., 2024, Vol 2, Issue 11, 417-424. https://doi.org/10.5281/zenodo.14054935