Originally conceived as harmful metabolic byproducts, reactive oxygen species (ROS) are now recognized as an integral part of numerous cellular programs. Thanks to their diverse physicochemical properties, compartmentalized production, and tight control exerted by the antioxidant machinery they activate signaling pathways that govern plant growth, development, and defense. Excessive ROS levels are often driven by adverse changes in environmental conditions, ultimately causing oxidative stress. The associated negative impact on cellular constituents have been a major focus of decade-long research efforts to improve the oxidative stress resilience by boosting the antioxidant machinery in model and crop species. We highlight the role of enzymatic and non-enzymatic antioxidants as integral factors of multiple signaling cascades beyond their mere function to prevent oxidative damage under adverse abiotic stress conditions.

• Klíčová slova
• antioxidants, oxidative stress, reactive oxygen species, stress resilience,
• MeSH
• antioxidancia metabolismus   MeSH
• fyziologický stres * MeSH
• fyziologie rostlin MeSH
• období sucha MeSH
• oxidace-redukce MeSH
• oxidační stres MeSH
• reaktivní formy kyslíku metabolismus   MeSH
• rostliny genetika   metabolismus   MeSH
• signální transdukce * MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• přehledy MeSH
• Názvy látek
• antioxidancia MeSH
• reaktivní formy kyslíku MeSH

Oxidative stress is a pathological process related to not only animal kingdom but also plants. Regarding oxidative stress in plants, heavy metals are frequently discussed as causative stimuli with relevance to ecology. Because heavy metals have broad technological importance, they can easily contaminate the environment. Much of previous effort regarding the harmful impact of the heavy metals was given to their toxicology in the animals and humans. Their implication in plant pathogeneses is less known and remains underestimated.The current paper summarizes basic facts about heavy metals, their distribution in soil, mobility, accumulation by plants, and initiation of oxidative stress including the decline in basal metabolism. The both actual and frontier studies in the field are summarized and discussed. The major pathophysiological pathways are introduced as well and link between heavy metals toxicity and their ability to initiate an oxidative damage is provided. Mobility and bioaccessibility of the metals is also considered as key factors in their impact on oxidative stress development in the plant. The metals like lead, mercury, copper, cadmium, iron, zinc, nickel, vanadium are depicted in the text.Heavy metals appear to be significant contributors to pathological processes in the plants and oxidative stress is probably an important contributor to the effect. The most sensitive plant species are enlisted and discussed in this review. The facts presented here outline next effort to investigate pathological processes in the plants.

• Klíčová slova
• Contamination, Heavy metals, Oxidative damage, Oxidative stress, Pathophysiological pathways, Plants,
• MeSH
• biologická dostupnost MeSH
• cukry metabolismus   MeSH
• druhová specificita MeSH
• oxidační stres účinky léků   MeSH
• rostliny metabolismus   MeSH
• těžké kovy metabolismus   toxicita   MeSH
• Publikační typ
• časopisecké články MeSH
• přehledy MeSH
• Názvy látek
• cukry MeSH
• těžké kovy MeSH

Fipronil (FIP) is widely used across the world as a broad-spectrum phenylpyrazole insecticide and veterinary drug. FIP was the insecticide to act by targeting the γ-aminobutyric acid (GABA) receptor and has favorable selective toxicity towards insects rather than mammals. However, because of accidental exposure, incorrect use of FIP or widespread FIP use leading to the contamination of water and soil, there is increasing evidence that FIP could cause a variety of toxic effects on animals and humans, such as neurotoxic, hepatotoxic, nephrotoxic, reproductive, and cytotoxic effects on vertebrate and invertebrates. In the last decade, oxidative stress has been suggested to be involved in the various toxicities induced by FIP. To date, few reviews have addressed the toxicity of FIP in relation to oxidative stress. The focus of this article is primarily intended to summarize the progress in research associated with oxidative stress as a possible mechanism for FIP-induced toxicity as well as metabolism. The present review reports that studies have been conducted to reveal the generation of reactive oxygen species (ROS) and oxidative stress as a result of FIP treatment and have correlated them with various types of toxicity. Furthermore, the metabolism of FIP was also reviewed, and during this process, various CYP450 enzymes were involved and oxidative stress might occur. The roles of various compounds in protecting against FIP-induced toxicity based on their anti-oxidative effects were also summarized to further understand the role of oxidative stress in FIP-induced toxicity.

• Klíčová slova
• Fipronil, ROS, antioxidants, insecticide, metabolism, oxidative stress, toxicology,
• MeSH
• insekticidy toxicita   MeSH
• látky znečišťující životní prostředí toxicita   MeSH
• lidé MeSH
• oxidace-redukce MeSH
• oxidační stres * MeSH
• pyrazoly toxicita   MeSH
• zvířata MeSH
• Check Tag
• lidé MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• přehledy MeSH
• Názvy látek
• fipronil MeSH Prohlížeč
• insekticidy MeSH
• látky znečišťující životní prostředí MeSH
• pyrazoly MeSH

Oxidative stress is the result of an imbalance between the formation of reactive oxygen species (ROS) and the levels of enzymatic and non-enzymatic antioxidants. The assessment of biological redox status is performed by the use of oxidative stress biomarkers. An oxidative stress biomarker is defined as any physical structure or process or chemical compound that can be assessed in a living being (in vivo) or in solid or fluid parts thereof (in vitro), the determination of which is a reproducible and reliable indicator of oxidative stress. The use of oxidative stress biomarkers allows early identification of the risk of developing diseases associated with this process and also opens up possibilities for new treatments. At the end of the last century, interest in oxidative stress biomarkers began to grow, due to evidence of the association between the generation of free radicals and various pathologies. Up to now, a significant number of studies have been carried out to identify and apply different oxidative stress biomarkers in clinical practice. Among the most important oxidative stress biomarkers, it can be mentioned the products of oxidative modifications of lipids, proteins, nucleic acids, and uric acid as well as the measurement of the total antioxidant capacity of fluids in the human body. In this review, we aim to present recent advances and current knowledge on the main biomarkers of oxidative stress, including the discovery of new biomarkers, with emphasis on the various reproductive complications associated with variations in oxidative stress levels.

• Klíčová slova
• Biomarker, Free radical, Oxidative stress, Reactive oxygen species, Reproductive complication,
• MeSH
• biologické markery MeSH
• fyzikální vyšetření MeSH
• lidé MeSH
• nukleové kyseliny * MeSH
• oxidační stres * MeSH
• reaktivní formy kyslíku MeSH
• Check Tag
• lidé MeSH
• Publikační typ
• časopisecké články MeSH
• přehledy MeSH
• Názvy látek
• biologické markery MeSH
• nukleové kyseliny * MeSH
• reaktivní formy kyslíku MeSH

Thousands of tons of neonicotinoids are widely used around the world as broad-spectrum systemic insecticides and veterinary drugs. Researchers originally thought that neonicotinoids exhibited low mammalian toxicity. However, following their widespread use, it became increasingly evident that neonicotinoids could have various toxic effects on vertebrates and invertebrates. The primary focus of this review is to summarize the research progress associated with oxidative stress as a plausible mechanism for neonicotinoid-induced toxicity as well as neonicotinoid metabolism. This review summarizes the research conducted over the past decade into the production of reactive oxygen species, reactive nitrogen species, and oxidative stress as aresult of neonicotinoid treatments, along with their correlation with the toxicity and metabolism of neonicotinoids. The metabolism of neonicotinoids and protection of various compounds against neonicotinoid-induced toxicity based on their antioxidative effects is also discussed. This review sheds new light on the critical roles of oxidative stress in neonicotinoid-induced toxicity to nontarget species.

• Klíčová slova
• ROS, clothianidin, imidacloprid, mechanisms, neonicotinoids, oxidative stress, thiamethoxam, toxicology,
• MeSH
• antioxidancia škodlivé účinky   farmakologie   MeSH
• insekticidy škodlivé účinky   farmakologie   MeSH
• lidé MeSH
• neonikotinoidy škodlivé účinky   farmakologie   MeSH
• oxidační stres účinky léků   MeSH
• zvířata MeSH
• Check Tag
• lidé MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• přehledy MeSH
• Názvy látek
• antioxidancia MeSH
• insekticidy MeSH
• neonikotinoidy MeSH

The role of oxidative stress in the physiopathology of human pregnancy is of particular interest. Pregnancy is well-known to increase the oxidative stress, mainly produced by a normal systemic inflammatory response, which results in high amounts of circulating reactive oxygen species (ROS) and reactive nitrogen species (RNS). Both ROS and RNS play an important role as secondary messengers in many intracellular signalling cascades. However, they can also exert critical effects on pathological processes involving the pregnant woman. ROS, RNS and antioxidants establish a balance that determines the oxidation status of animals and humans. This review focuses on the mechanism of oxidative stress in pregnancy as well as its involvement and consequences on the human pregnancy-specific clinical syndrome preeclampsia.

• Klíčová slova
• Oxidative stress, Preeclampsia, RNS, ROS,
• MeSH
• antioxidancia terapeutické užití   MeSH
• endoteliální buňky metabolismus   MeSH
• ischemie metabolismus   MeSH
• lidé MeSH
• melatonin metabolismus   MeSH
• oxidace-redukce MeSH
• oxidační stres fyziologie   MeSH
• placenta metabolismus   MeSH
• preeklampsie farmakoterapie   metabolismus   MeSH
• reaktivní formy dusíku metabolismus   MeSH
• reaktivní formy kyslíku metabolismus   MeSH
• signální transdukce MeSH
• těhotenství metabolismus   MeSH
• volné radikály MeSH
• zvířata MeSH
• Check Tag
• lidé MeSH
• těhotenství metabolismus   MeSH
• ženské pohlaví MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• přehledy MeSH
• Názvy látek
• antioxidancia MeSH
• melatonin MeSH
• reaktivní formy dusíku MeSH
• reaktivní formy kyslíku MeSH
• volné radikály MeSH

According to the United States Centers for Disease Control and Prevention (CDC), as of July 11, 2016, the reported average incidence of children diagnosed with an autism spectrum disorder (ASD) was 1 in 68 (1.46%) among 8-year-old children born in 2004 and living within the 11 monitoring sites' surveillance areas in the United States of America (USA) in 2012. ASD is a multifaceted neurodevelopmental disorder that is also considered a hidden disability, as, for the most part; there are no apparent morphological differences between children with ASD and typically developing children. ASD is diagnosed based upon a triad of features including impairment in socialization, impairment in language, and repetitive and stereotypic behaviors. The increasing incidence of ASD in the pediatric population and the lack of successful curative therapies make ASD one of the most challenging disorders for medicine. ASD neurobiology is thought to be associated with oxidative stress, as shown by increased levels of reactive oxygen species and increased lipid peroxidation, as well as an increase in other indicators of oxidative stress. Children with ASD diagnosis are considered more vulnerable to oxidative stress because of their imbalance in intracellular and extracellular glutathione levels and decreased glutathione reserve capacity. Several studies have suggested that the redox imbalance and oxidative stress are integral parts of ASD pathophysiology. As such, early assessment and treatment of antioxidant status may result in a better prognosis as it could decrease the oxidative stress in the brain before it can induce more irreversible brain damage. In this review, many aspects of the role of oxidative stress in ASD are discussed, taking into account that the process of oxidative stress may be a target for therapeutic interventions.

• Klíčová slova
• ASD, Autism, Inflammation, Oxidative stress, Reactive oxygen species,
• MeSH
• aerobióza MeSH
• antioxidancia metabolismus   MeSH
• centrální nervový systém metabolismus   MeSH
• dítě MeSH
• dysbióza komplikace   MeSH
• gastrointestinální nemoci komplikace   MeSH
• glutathionperoxidasa metabolismus   MeSH
• incidence MeSH
• lidé MeSH
• metalothionein metabolismus   MeSH
• mitochondrie metabolismus   MeSH
• mozek - chemie MeSH
• neurodegenerativní nemoci etiologie   metabolismus   MeSH
• oxidace-redukce MeSH
• oxidační stres * MeSH
• peroxidace lipidů MeSH
• poruchy autistického spektra epidemiologie   imunologie   metabolismus   patofyziologie   MeSH
• předškolní dítě MeSH
• scavengery volných radikálů metabolismus   MeSH
• selen fyziologie   MeSH
• selenoproteiny metabolismus   MeSH
• střevní mikroflóra MeSH
• Check Tag
• dítě MeSH
• lidé MeSH
• předškolní dítě MeSH
• Publikační typ
• časopisecké články MeSH
• přehledy MeSH
• Názvy látek
• antioxidancia MeSH
• glutathionperoxidasa MeSH
• metalothionein MeSH
• scavengery volných radikálů MeSH
• selen MeSH
• selenoproteiny MeSH

Statins, 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitors, are currently the most effective lipid-lowering drugs, effectively reducing the plasma total cholesterol and low-density lipoprotein, while also decreasing three triacylglycerols and increasing plasma high-density lipoprotein to a certain extent. However, the excessive or long-term use of statins can cause in vitro cytotoxicity, in vivo liver injury, liver necrosis, kidney damage, and myopathy in both human beings and animals. Many studies indicate that oxidative stress is involved in the various toxicities associated with statins, and various antioxidants have been evaluated to investigate their protective roles against statin-induced liver, kidney, and muscle toxicities. Widespread attention has been given to statin-induced oxidative stress, with and without the use of other drugs. Much of the information about the mechanism for this reduction comes from cell culture and in experimental animal studies. The primary focus of this article is to summarize the research progress associated with oxidative stress as a plausible mechanism for statin-induced toxicity, as well as its metabolic interactions. This review summarizes the research conducted over the past five years into the production of reactive oxygen species, oxidative stress as a result of statin treatments, and their correlation with statin-induced toxicity and metabolism. Statin-induced metabolism involves various CYP450 enzymes, which provide potential sites for statin-induced oxidative stress, and these metabolic factors are also reviewed. The therapeutics of a variety of compounds against statin-induced organ damage based on their anti-oxidative effects is also discussed to further understand the role of oxidative stress in statin-induced toxicity. This review sheds new light on the critical roles of oxidative stress in statin-induced toxicity and prevention of this oxidative damage, as well as on the contradictions and unknowns that still exist regarding statin toxicity and the cellular effects in terms of organ injury and cell signaling pathways.

• Klíčová slova
• Metabolic interaction, Oxidative stress, Statins, Toxicology,
• MeSH
• lékové interakce MeSH
• lidé MeSH
• oxidační stres účinky léků   MeSH
• předávkování léky MeSH
• statiny škodlivé účinky   farmakokinetika   MeSH
• zvířata MeSH
• Check Tag
• lidé MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• přehledy MeSH
• Názvy látek
• statiny MeSH

Despite the main mechanism of organophosphate (OP) toxicity through inhibition of acetylcholinesterase (AChE) being well known over the years, some chronic adverse health effects indicate the involvement of additional pathways. Oxidative stress is among the most intensively studied. Overstimulation of cholinergic and glutamatergic nervous system is followed by intensified generation of reactive species and oxidative damage in many tissues. In this review, the role of oxidative stress in pathophysiology of OP poisoning and the influence of commonly used medical interventions on its levels are discussed. Current standardized therapy of OP intoxications comprises live-saving administration of the anticholinergic drug atropine accompanied by oxime AChE reactivator and diazepam. The capability of these antidotes to ameliorate OP-induced oxidative stress varies between both therapeutic groups and individual medications within the drug class. Regarding oxidative stress, atropine does not seem to have a significant effect on oxidative stress parameters in OP poisoning. In a case of AChE reactivators, pro-oxidative and antioxidative properties could be found. It is assumed that the ability of oximes to trigger oxidative stress is rather associated with their chemical structure than reactivation efficacy. The data indicating the potency of diazepam in preventing OP-induced oxidative stress are not available. Based on current knowledge on the mechanism of OP-mediated oxidative stress, alternative approaches (including antioxidants or multifunctional drugs) in therapy of OP poisoning are under consideration.

• Klíčová slova
• antidotes, atropine, diazepam, nerve agents, organophosphate, oxidative stress, oximes, pesticide,
• MeSH
• antidota terapeutické užití   MeSH
• antioxidancia terapeutické užití   MeSH
• atropin terapeutické užití   MeSH
• diazepam terapeutické užití   MeSH
• lidé MeSH
• otrava organofosfáty farmakoterapie   MeSH
• oxidační stres účinky léků   MeSH
• oximy terapeutické užití   MeSH
• reaktivátory cholinesterázy terapeutické užití   MeSH
• zvířata MeSH
• Check Tag
• lidé MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• přehledy MeSH
• Názvy látek
• antidota MeSH
• antioxidancia MeSH
• atropin MeSH
• diazepam MeSH
• oximy MeSH
• reaktivátory cholinesterázy MeSH

Oxidative stress is a phenomenon associated with pathogenetic mechanisms of several diseases including atherosclerosis, neurodegenerative diseases, such as Alzheimer's and Parkinson's disease, cancer, diabetes mellitus, inflammatory diseases, as well as psychological diseases or aging processes. Oxidative stress is defined as an imbalance between production of free radicals and reactive metabolites, so-called oxidants, and their elimination by protective mechanisms, referred to as antioxidative systems. This imbalance leads to damage of important biomolecules and organs with potential impact on the whole organism. Oxidative and antioxidative processes are associated with electron transfer influencing the redox state of cells and the organism. The changed redox state stimulates or inhibits activities of various signal proteins, resulting in a changed ability of signal pathways to influence the fate of cells. At present, the opinion that oxidative stress is not always harmful, has been accepted. Depending on the type of oxidants, intensity and time of redox imbalance as well as on the type of cells, oxidative stress can play a role in the regulation of other important processes through modulation of signal pathways, influencing synthesis of antioxidant enzymes, repair processes, inflammation, apoptosis and cell proliferation, and thus processes of malignity. Imprudent administration of antioxidants may therefore have a negative impact on the organism.

• MeSH
• antioxidancia metabolismus   MeSH
• homeostáza MeSH
• lidé MeSH
• oxidace-redukce MeSH
• oxidační stres * MeSH
• reaktivní formy kyslíku metabolismus   MeSH
• signální transdukce MeSH
• zvířata MeSH
• Check Tag
• lidé MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• přehledy MeSH
• Názvy látek
• antioxidancia MeSH
• reaktivní formy kyslíku MeSH