Irma Ares

Bio: Irma Ares is an academic researcher from Complutense University of Madrid. The author has contributed to research in topics: Oxidative stress & Toxicity. The author has an hindex of 21, co-authored 75 publications receiving 1280 citations.

Mechanism of Neonicotinoid Toxicity: Impact on Oxidative Stress and Metabolism

Abstract: 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.

Fipronil insecticide toxicology: oxidative stress and metabolism

Abstract: 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.

Mammalian caspases: structure ,a ctivation ,s ubstrates, and functions during apoptosis

Abstract: ■ Abstract Apoptosis is a genetically programmed, morphologically distinct form of cell death that can be triggered by a variety of physiological and pathological stimuli. Studies performed over the past 10 years have demonstrated that proteases play critical roles in initiation and execution of this process. The caspases, a family of cysteine-dependent aspartate-directed proteases, are prominent among the death proteases. Caspases are synthesized as relatively inactive zymogens that become activated by scaffold-mediated transactivation or by cleavage via upstream proteases in an intracellular cascade. Regulation of caspase activation and activity occurs at several different levels: ( a) Zymogen gene transcription is regulated; ( b) antiapoptotic members of the Bcl-2 family and other cellular polypeptides block proximity-induced activation of certain procaspases; and ( c) certain cellular inhibitor of apoptosis proteins (cIAPs) can bind to and inhibit active caspases. Once activated, caspases cleave a variety of intracellular polypeptides, including major structural elements of the cytoplasm and nucleus, components of the DNA repair machinery, and a number of protein kinases. Collectively, these scissions disrupt survival pathways and disassemble important architectural components of the cell, contributing to the stereotypic morphological and biochemical changes that characterize apoptotic cell death.

Food Protein‐Derived Bioactive Peptides: Production, Processing, and Potential Health Benefits

Abstract: Bioactive peptides (BAPs), derived through enzymatic hydrolysis of food proteins, have demonstrated potential for application as health-promoting agents against numerous human health and disease conditions, including cardiovascular disease, inflammation, and cancer. The feasibility of pharmacological application of these peptides depends on absorption and bioavailability in intact forms in target tissues, which in turn depends on structure of the peptides. Therefore, production and processing of peptides based on important structure-function parameters can lead to the production of potent peptides. This article reviews the literature on BAPs with emphasis on strategic production and processing methods as well as antihypertensive, anticancer, anticalmodulin, hypocholesterolemic, and multifunctional properties of the food protein-derived peptides. It is recommended that future research efforts on BAP should be directed toward elucidation of their in vivo molecular mechanisms of action, safety at various doses, and pharmacological activity in maintaining homeostasis during aberrant health conditions in human subjects.

Melatonin, a Full Service Anti-Cancer Agent: Inhibition of Initiation, Progression and Metastasis.

Abstract: There is highly credible evidence that melatonin mitigates cancer at the initiation, progression and metastasis phases. In many cases, the molecular mechanisms underpinning these inhibitory actions have been proposed. What is rather perplexing, however, is the large number of processes by which melatonin reportedly restrains cancer development and growth. These diverse actions suggest that what is being observed are merely epiphenomena of an underlying more fundamental action of melatonin that remains to be disclosed. Some of the arresting actions of melatonin on cancer are clearly membrane receptor-mediated while others are membrane receptor-independent and involve direct intracellular actions of this ubiquitously-distributed molecule. While the emphasis of melatonin/cancer research has been on the role of the indoleamine in restraining breast cancer, this is changing quickly with many cancer types having been shown to be susceptible to inhibition by melatonin. There are several facets of this research which could have immediate applications at the clinical level. Many studies have shown that melatonin’s co-administration improves the sensitivity of cancers to inhibition by conventional drugs. Even more important are the findings that melatonin renders cancers previously totally resistant to treatment sensitive to these same therapies. Melatonin also inhibits molecular processes associated with metastasis by limiting the entrance of cancer cells into the vascular system and preventing them from establishing secondary growths at distant sites. This is of particular importance since cancer metastasis often significantly contributes to death of the patient. Another area that deserves additional consideration is related to the capacity of melatonin in reducing the toxic consequences of anti-cancer drugs while increasing their efficacy. Although this information has been available for more than a decade, it has not been adequately exploited at the clinical level. Even if the only beneficial actions of melatonin in cancer patients are its ability to attenuate acute and long-term drug toxicity, melatonin should be used to improve the physical wellbeing of the patients. The experimental findings, however, suggest that the advantages of using melatonin as a co-treatment with conventional cancer therapies would far exceed improvements in the wellbeing of the patients.

Pesticide toxicity: a mechanistic approach.

Abstract: Pesticides are known for their high persistence and pervasiveness in the environment, and along with products of their biotransformation, they may remain in and interact with the environment and living organisms in multiple ways, according to their nature and chemical structure, dose and targets. In this review, the classifications of pesticides based on their nature, use, physical state, pathophysiological effects, and sources are discussed. The effects of these xenobiotics on the environment, their biotransformation in terms of bioaccumulation are highlighted with special focus on the molecular mechanisms deciphered to date. Basing on targeted organisms, most pesticides are classified as herbicides, fungicides, and insecticides. Herbicides are known as growth regulators, seedling growth inhibitors, photosynthesis inhibitors, inhibitors of amino acid and lipid biosynthesis, cell membrane disrupters, and pigment biosynthesis inhibitors, whereas fungicides include inhibitors of ergosterol biosynthesis, protein biosynthesis, and mitochondrial respiration. Insecticides mainly affect nerves and muscle, growth and development, and energy production. Studying the impact of pesticides and other related chemicals is of great interest to animal and human health risk assessment processes since potentially everyone can be exposed to these compounds which may cause many diseases, including metabolic syndrome, malnutrition, atherosclerosis, inflammation, pathogen invasion, nerve injury, and susceptibility to infectious diseases. Future studies should be directed to investigate influence of long term effects of low pesticide doses and to minimize or eliminate influence of pesticides on non-target living organisms, produce more specific pesticides and using modern technologies to decrease contamination of food and other goods by pesticides.