Mechanistic Role of Reactive Oxygen Species and Its Regulation Via the Antioxidant System under Environmental Stress

The antioxidant potential is referred to as compounds that are capable of protecting the biological system against the deleterious effect of reactions involving reactive oxygen species (ROS). ROS are toxic byproducts of oxygen metabolism. ROS have a significant role in plant signaling, growth, development, and majorly in response to environmental fluctuations. The ROS family plays a double role under various environmental stress conditions. In various key physiological phenomena, they act as secondary messengers and induce oxidative damage. ROS led to cellular damages that manifest themselves in degradation of biomolecules, which eventually amalgamate to cellular death in plants. To assure survival, plants have developed efficient antioxidant machinery having two branches, that is, an enzymatic and a nonenzymatic antioxidant. This chapter will emphasize the various types of ROS, their sites of cellular production, targets, and scavenging mechanisms mediated by antioxidants in abiotic stress. Such profound knowledge will let us build strategies against environmental stress.

Reactive Oxygen Species as the Brainbox in Malaria Treatment

Several measures are in place to combat the worldwide spread of malaria, especially in regions of high endemicity. In part, most common antimalarials, such as quinolines and artemisinin and its derivatives, deploy an ROS-mediated approach to kill malaria parasites. Although some antimalarials may share similar targets and mechanisms of action, varying levels of reactive oxygen species (ROS) generation may account for their varying pharmacological activities. Regardless of the numerous approaches employed currently and in development to treat malaria, concerningly, there has been increasing development of resistance by Plasmodium falciparum, which can be connected to the ability of the parasites to manage the oxidative stress from ROS produced under steady or treatment states. ROS generation has remained the mainstay in enforcing the antiparasitic activity of most conventional antimalarials. However, a combination of conventional drugs with ROS-generating ability and newer drugs that exploit vital metabolic pathways, such antioxidant machinery, could be the way forward in effective malaria control.

Seed priming of plants aiding in drought stress tolerance and faster recovery: a review

Drought stress exposure adversely affects plant growth and productivity. Various seed priming techniques are experimented to mitigate the adverse effect of drought stress on plant performance. It is a low-cost and sustainable technology that proved to be of immense potential to enhance drought tolerance and increase crop productivity. Drought episodes are followed by recovery through rain or irrigation and help the plants to recuperate from the damages caused by drought stress. The severity of drought-associated damages determines the recovery kinetics of plants. Under the recurrent cycle of drought events, recovery kinetics has immense importance in predicting the stress tolerance potential and survival status of a plant. Many processes like DNA damage repair, de-novo synthesis of nucleic acids and proteins, osmotic adjustment through the accumulation of osmolytes, the potential activity of antioxidant machinery occurring during seed priming play a significant role during recovery from drought stress. Alleviation of the severity of drought stress through the accumulation of osmolytes, the augmented activity of antioxidant machinery, improved photosynthetic performance, and the upregulated expression of stress-responsive genes attributed by seed priming will complement the recovery from drought stress. Although the beneficial effects of seed priming on drought tolerance are well explored, priming influenced recovery mechanism has not been well explored. There is a lacuna in the field of research related to the beneficial effects of seed priming for recovery from drought stress, and that is the focus of this paper.

Superoxide Dismutase Administration: A Review of Proposed Human Uses

Superoxide dismutases (SODs) are metalloenzymes that play a major role in antioxidant defense against oxidative stress in the body. SOD supplementation may therefore trigger the endogenous antioxidant machinery for the neutralization of free-radical excess and be used in a variety of pathological settings. This paper aimed to provide an extensive review of the possible uses of SODs in a range of pathological settings, as well as describe the current pitfalls and the delivery strategies that are in development to solve bioavailability issues. We carried out a PubMed query, using the keywords “SOD”, “SOD mimetics”, “SOD supplementation”, which included papers published in the English language, between 2012 and 2020, on the potential therapeutic applications of SODs, including detoxification strategies. As highlighted in this paper, it can be argued that the generic antioxidant effects of SODs are beneficial under all tested conditions, from ocular and cardiovascular diseases to neurodegenerative disorders and metabolic diseases, including diabetes and its complications and obesity. However, it must be underlined that clinical evidence for its efficacy is limited and consequently, this efficacy is currently far from being demonstrated.

Frataxins Emerge as New Players of the Intracellular Antioxidant Machinery

Frataxin is a mitochondrial protein which deficiency causes Friedreich’s ataxia, a cardio-neurodegenerative disease. The lack of frataxin induces the dysregulation of mitochondrial iron homeostasis and oxidative stress, which finally causes the neuronal death. The mechanism through which frataxin regulates the oxidative stress balance is rather complex and poorly understood. While the absence of human (Hfra) and yeast (Yfh1) frataxins turn out cells sensitive to oxidative stress, this does not occur when the frataxin gene is knocked-out in E. coli. To better understand the biological roles of Hfra and Yfh1 as endogenous antioxidants, we have studied their ability to inhibit the formation of reactive oxygen species (ROS) from Cu2+- and Fe3+-catalyzed degradation of ascorbic acid. Both proteins drastically reduce the formation of ROS, and during this process they are not oxidized. In addition, we have also demonstrated that merely the presence of Yfh1 or Hfra is enough to protect a highly oxidation-prone protein such as α-synuclein. This unspecific intervention (without a direct binding) suggests that frataxins could act as a shield to prevent the oxidation of a broad set of intracellular proteins, and reinforces that idea that frataxin can be used to prevent neurological pathologies linked to an enhanced oxidative stress.