A review of poisoning with various types of biotoxins and its common clinical symptoms.

INTRODUCTION: Biotoxins are toxic substances that originate from living organisms and are harmful to humans. Therefore, we need to know the symptoms of biotoxins poisoning to manage the damage. The purpose of this study is to establish a practical diagnostic protocol for dealing with poisoned patients exposed to biotoxins. MATERIALS AND METHODS: The present study is a review study. Our studied community is articles and books matching the title of the project and relevant keywords. First, by searching the key words sign, symptom, biotoxins, relevant articles were extracted and studied from valid databases. By reviewing the studies based on the search strategy, four groups of biotoxins that were studied the most were identified. These four groups are marine biotoxins, bacterial biotoxins, fungal biotoxins and plant biotoxins. In each of these biotoxin groups, important toxins were selected and studied. RESULTS: A total of 1864 articles were initially identified from the databases searched in present study. After screening titles and abstracts, 26 articles were included in the systematic review. Specifically, 7 articles were included for bacterial toxins, 9 articles for marine toxins, 5 articles for plant toxins and 5 articles for fungal toxins. CONCLUSION: The symptoms of plant biotoxins poisoning may include cardiovascular, hematologic, neurologic, respiratory, renal, and gastrointestinal symptoms, while the symptoms of fungal biotoxins poisoning may include hepatic, renal, gastrointestinal, musculoskeletal, metabolic, respiratory, neurological, and cardiovascular symptoms. marine biotoxins poisoning presents with gastrointestinal and neurological symptoms, with varying incubation periods and recovery times. bacterial biotoxins exposure can lead to a wide range of clinical symptoms, with diarrhea, vomiting, and abdominal pain being the most common, and hemoglobinuria or hematuria being a sensitive and specific clinical manifestation for diagnosing ongoing HUS in children.

The controversial effect of smoking and nicotine in SARS-CoV-2 infection.

The effects of nicotine and cigarette smoke in many diseases, notably COVID-19 infection, are being debated more frequently. The current basic data for COVID-19 is increasing and indicating the higher risk of COVID-19 infections in smokers due to the overexpression of corresponding host receptors to viral entry. However, current multi-national epidemiological reports indicate a lower incidence of COVID-19 disease in smokers. Current data indicates that smokers are more susceptible to some diseases and more protective of some other. Interestingly, nicotine is also reported to play a dual role, being both inflammatory and anti-inflammatory. In the present study, we tried to investigate the effect of pure nicotine on various cells involved in COVID-19 infection. We followed an organ-based systematic approach to decipher the effect of nicotine in damaged organs corresponding to COVID-19 pathogenesis (12 related diseases). Considering that the effects of nicotine and cigarette smoke are different from each other, it is necessary to be careful in generalizing the effects of nicotine and cigarette to each other in the conducted researches. The generalization and the undifferentiation of nicotine from smoke is a significant bias. Moreover, different doses of nicotine stimulate different effects (dose-dependent response). In addition to further assessing the role of nicotine in COVID-19 infection and any other cases, a clever assessment of underlying diseases should also be considered to achieve a guideline for health providers and a personalized approach to treatment.

Changes in DNA methylation in APOE and ACKR3 genes in multiple sclerosis patients and the relationship with their heavy metal blood levels.

Multiple sclerosis (MS) is a chronic inflammatory disease with demyelinated lesions in the central nervous system caused by genetic and environmental factors. DNA methylation as an epigenetic change influenced by environmental factors, including heavy metals has been implemented in MS disease. We investigated the correlation of DNA methylation changes in APOE and ACKR3 genes in MS patients and the possible association with blood concentration of arsenic (As), cadmium (Cd) and lead (Pb) as major heavy metal pollutants. This study included 69 relapsing-remitting multiple sclerosis (RR-MS) patients and 69 age/gender-matched healthy subjects. The HRM real-time PCR method was used to investigate the changes in DNA methylation and heavy metal concentrations were measured by electrothermal atomic absorption spectrometry. Our results showed that the methylation pattern in the ACKR3 gene of the patient group was more hypomethylated, while in the case of the APOE gene, this pattern was more towards hypermethylation compared to healthy subjects. Moreover, the blood levels of As and Cd metals, but not Pb, were significantly higher in the patient group compare to the control group (p ≤ 0.05). The data indicate that the increase in expression of ACKR3 gene by hypomethylation and the decrease in expression of APOE gene via hypermethylation are possibly involved in the onset and progression of inflammatory processes in MS patients. The level of As can also lead to hypomethylation by disrupting the methylation patterns of the ACKR3 gene, resulting in increased expression in MS patients. Finally, we have shown that epigenetic changes can be an important factor in increasing and decreasing the expression of genes involved in the onset and/or progression of inflammatory processes in MS. Furthermore, exposure to heavy metals, especially As, by changing the natural patterns of DNA methylation can be effective in this disease.

Mechanisms and pathogenesis underlying environmental chemical-induced necroptosis.

Necroptosis is a regulated cell death that is governed by mixed lineage kinase domain-like, receptor-interacting serine-threonine kinase 3 and commonly displays with necrosis morphological characteristics. This study examined the molecular mechanisms involved in the chemical-induced necroptosis where a systematic evaluation of experimental studies addressing this issue is missing. We strictly reviewed all scientific reports related to our search terms including "necroptosis" or "programmed necrosis", "environmental chemicals" or "air pollutants" or "pesticides" or "nanoparticles" and "Medicines" from 2009 to 2019. Manuscripts that met the objective of this study were included for further evaluations. Studies showed that several pathological contexts like cancer, neurodegenerative disorders, and inflammatory diseases were related to necroptosis. Furthermore, multiple chemical-induced cytotoxic effects, such as DNA damage, mitochondrial dysregulation, oxidative damage, lipid peroxidation, endoplasmic reticulum disruption, and inflammation are also associated with necroptosis. The main environmental exposures that are related to necroptosis are air pollutants (airborne particulate matter, cadmium, and hydrogen sulfide), nanoparticles (gold, silver, and silica), pesticides (endosulfan, cypermethrin, chlorpyrifos, and paraquat), and tobacco smoke. To sum up, air pollutants, pesticides, and nanoparticles could potentially affect human health via disruption of cell growth and induction of necroptosis. Understanding the exact molecular pathogenesis of these environmental chemicals needs further comprehensive research to provide innovative concepts for the prevention approaches and introduce novel targets for the amelioration of a range of human health problems.