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Raman microspectroscopy was tested as an alternative/complementary method for biochemical evaluation of the synaptosomes obtained from neonatal rat brain prenatally exposed to sodium valproate and treated with allicin. Spectrophotometric assays of several oxidative stress markers (catalase, superoxide dismutase, total thiols) and acetylcholine esterase activity revealed the redox balancing function and pro-cholinergic effect of the allicin as compared to the valproate effect. Raman evaluation showed no significant changes in our experimental conditions. Different concentrations and volumes of the synaptosomes vesicles must be tested for the optimal Raman examination of these purified synaptosomes.

• A highly negative glutathione redox potential (EGSH ) is maintained in the cytosol, plastids and mitochondria of plant cells to support fundamental processes, including antioxidant defence, redox regulation and ironasulfur cluster biogenesis. Out of two glutathione reductase (GR) proteins in Arabidopsis, GR2 is predicted to be dual-targeted to plastids and mitochondria, but its differential roles in these organelles remain unclear. • We dissected the role of GR2 in organelle glutathione redox homeostasis and plant development using a combination of genetic complementation and stacked mutants, biochemical activity studies, immunogold labelling and in vivo biosensing. • Our data demonstrate that GR2 is dual-targeted to plastids and mitochondria, but embryo lethality of gr2 null mutants is caused specifically in plastids. Whereas lack of mitochondrial GR2 leads to a partially oxidised glutathione pool in the matrix, the ATP-binding cassette (ABC) transporter ATM3 and the mitochondrial thioredoxin system provide functional backup and maintain plant viability. • We identify GR2 as essential in the plastid stroma, where it counters GSSG accumulation and developmental arrest. By contrast a functional triad of GR2, ATM3 and the thioredoxin system in the mitochondria provides resilience to excessive glutathione oxidation.

Heavy metal (HM) toxicity has become a global concern in recent years and is imposing a severe threat to the environment and human health. In the case of plants, a higher concentration of HMs, above a threshold, adversely affects cellular metabolism because of the generation of reactive oxygen species (ROS) which target the key biological molecules. Moreover, some of the HMs such as mercury and arsenic, among others, can directly alter the protein/enzyme activities by targeting their –SH group to further impede the cellular metabolism. Particularly, inhibition of photosynthesis has been reported under HM toxicity because HMs trigger the degradation of chlorophyll molecules by enhancing the chlorophyllase activity and by replacing the central Mg ion in the porphyrin ring which affects overall plant growth and yield. Consequently, plants utilize various strategies to mitigate the negative impact of HM toxicity by limiting the uptake of these HMs and their sequestration into the vacuoles with the help of various molecules including proteins such as phytochelatins, metallothionein, compatible solutes, and secondary metabolites. In this comprehensive review, we provided insights towards a wider aspect of HM toxicity, ranging from their negative impact on plant growth to the mechanisms employed by the plants to alleviate the HM toxicity and presented the molecular mechanism of HMs toxicity and sequestration in plants.

Phyto-melatonin improves crop yield by mitigating the negative effects of abiotic stresses on plant growth. Numerous studies are currently being conducted to investigate the significant performance of melatonin in crops in regulating agricultural growth and productivity. However, a comprehensive review of the pivotal performance of phyto-melatonin in regulating plant morpho-physiological and biochemical activities under abiotic stresses needs to be clarified. This review focused on the research on morpho-physiological activities, plant growth regulation, redox status, and signal transduction in plants under abiotic stresses. Furthermore, it also highlighted the role of phyto-melatonin in plant defense systems and as biostimulants under abiotic stress conditions. The study revealed that phyto-melatonin enhances some leaf senescence proteins, and that protein further interacts with the plant’s photosynthesis activity, macromolecules, and changes in redox and response to abiotic stress. Our goal is to thoroughly evaluate phyto-melatonin performance under abiotic stress, which will help us better understand the mechanism by which phyto-melatonin regulates crop growth and yield.

Reactive oxygen species and oxidative stress are closely associated with various pathologies such as neurodegenerative diseases, ageing and male infertility. Hence, antioxidants such as vitamin C, vitamin E, N‐acetyl cysteine, L‐carnitine and folic acid are regularly used in various treatment regimens to protect cells from the damage induced by free radicals. However, given their over‐the‐counter availability at unnaturally high concentrations and also the fact that they are commonly added to various food products, patients may run a risk of consuming excessive dosages of these compounds, which may then be toxic. The few studies that have assessed antioxidant overuse and the associated adverse effects found that large doses of dietary antioxidant supplements have varying—if any—therapeutic effects even though free radicals clearly damage cells—a phenomenon that has been termed the “antioxidant paradox.” Furthermore, overuse of antioxidants such as vitamin C, vitamin E, N‐acetyl cysteine may lead to reductive stress, which is reported to be as dangerous to cells as oxidative stress and can be the cause of diseases such as cancer or cardiomyopathy. Therefore, we feel that there is a need for more elaborate research to establish the clear benefits and risks involved in antioxidant therapy for male infertility.

Se is a micronutrient essential for human health. Sub-optimal Se status is common, occurring in a significant proportion of the population across the world including parts of Europe and China. Human and animal studies have shown that Se status is a key determinant of the host response to viral infections. In this review, we address the question whether Se intake is a factor in determining the severity of response to coronavirus disease 2019 (COVID-19). Emphasis is placed on epidemiological and animal studies which suggest that Se affects host response to RNA viruses and on the molecular mechanisms by which Se and selenoproteins modulate the inter-linked redox homeostasis, stress response and inflammatory response. Together these studies indicate that Se status is an important factor in determining the host response to viral infections. Therefore, we conclude that Se status is likely to influence human response to the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection and that Se status is one (of several) risk factors which may impact on the outcome of SARS-CoV-2 infection, particularly in populations where Se intake is sub-optimal or low. We suggest the use of appropriate markers to assess the Se status of COVID-19 patients and possible supplementation may be beneficial in limiting the severity of symptoms, especially in countries where Se status is regarded as sub-optimal.

Glucocorticoids released from the adrenal gland in response to stress-induced activation of the hypothalamic-pituitary-adrenal (HPA) axis induce activity in the cellular reduction-oxidation (redox) system. The redox system is a ubiquitous chemical mechanism allowing the transfer of electrons between donor/acceptors and target molecules during oxidative phosphorylation while simultaneously maintaining the overall cellular environment in a reduced state. The objective of this review is to present an overview of the current literature discussing the link between HPA axis-derived glucocorticoids and increased oxidative stress, particularly focussing on the redox changes observed in the hippocampus following glucocorticoid exposure.

Amyotrophic lateral sclerosis (ALS) is the most common neurodegenerative disease of the motor system. It is characterized by the degeneration of both upper and lower motor neurons, which leads to muscle weakness and paralysis. ALS is incurable and has a bleak prognosis, with median survival of 3–5 years after the initial symptomatology. In ALS, motor neurons gradually degenerate and die. Many features of mitochondrial dysfunction are manifested in neurodegenerative diseases, including ALS. Mitochondria have shown to be an early target in ALS pathophysiology and contribute to disease progression. Disruption of their axonal transport, excessive generation of reactive oxygen species, disruption of the mitochondrial structure, dynamics, mitophagy, energy production, calcium buffering and apoptotic triggering have all been directly involved in disease pathogenesis and extensively reported in ALS patients and animal model systems. Alterations in energy production by motor neurons, which severely limit their survival capacity, are tightly linked to the redox status and mitochondria. The present review focuses on this link. Placing oxidative stress as a main pathophysiological mechanism, the molecular interactions and metabolic flows involved are analyzed. This leads to discussing potential therapeutic approaches targeting mitochondrial biology to slow disease progression.

Cellular redox status presents broad implications with diverse physiological and pathological processes. Simultaneous detection of both the oxidative and reductive species of redox couples, especially the most representative pair glutathione/hydrogen peroxide (GSH/H 2 O 2 ), is crucial to accurately map the cellular redox status. However, it still remains challenging to synchronously detect GSH/H 2 O 2 in vivo due to lack of a reliable measuring tool. Herein, a ratiometric nanoprobe (UCNP-TB) possessing simultaneous delectability of GSH/H 2 O 2 is established based on a multi-spectral upconverting nanophosphor (UCNP-OA) as the luminescence resonance energy transfer (LRET) donor and two dye molecules as the acceptors, including a GSH-sensitive dye (TCG) and a H 2 O 2 -sensitive dye (BCH). With the as-prepared UCNP-TB, real-time and synchronous monitoring the variation of GSH and H 2 O 2 in vitro and in living mice can be achieved using the ratio of the upconversion luminescence (UCL) at 540 and 650 nm to that at 800 nm as the detection signal, respectively, providing highly inherent reliability of the sensing results by self-calibration. Moreover, the nanoprobe is capable of mapping the redox status within the drug-resistant tumor and the drug-induced hepatotoxic liver via ratiometric UCL imaging. Thus, this nanoprobe would provide a reliable tool to elucidate the redox state in vivo .

Epilepsy is an intricate neurological disease where the neurons are severely affected, leading to the mortality of millions worldwide. Status epilepticus (SE), induced by lithium chloride (LiCl) and pilocarpine, is the most accepted model for epilepsy. The current work aims to unravel the mechanisms underlying the anti-epileptic efficacy of zingerone (an active ingredient of ginger), which has beneficial pharmacological activities on seizure-induced behavioral, histological, neurochemical, and molecular patterns in mice. Zingerone restored cognitive function by diminishing seizure activity, escape latency, and subsequent hippocampal damage manifested in histology. Seizures are associated with local inflammation, redox imbalance, and neural loss, confirmed by the present study of SE, and was attenuated by zingerone treatment. Nuclear factor-kappa B and its downstream signaling molecules (TNF-α, IL-1β, IL-6, NO, MPO) were activated in the LiCl-and-pilocarpine-induced group leading to inflammatory signaling, which was substantially ameliorated by zingerone treatment. The intrinsic apoptotic process was triggered subsequent to SE, as demonstrated by augmentation of cleaved caspase-3, downregulation of Bcl-2. However, zingerone treatment downregulated caspase-3 and upregulated Bcl-2, increasing cell survival and decreasing hippocampal neural death, deciphering involvement of apoptosis in SE. Therefore, zingerone plays an essential role in neuroprotection, probably by precluding oxidative stress, inflammation, and obstructing the mitochondrial pathway of apoptosis.