“…The current study was carried out on 60 Swiss albino male mice aged 6–8 weeks and weighing approximately 20–25 g, which were obtained from the animal house of faculty of Pharmacy at Isfahan University of Medical Sciences, Iran. The animals were kept in controlled conditions at a temperature of 20 ± 2 °C, humidity of about 50–60 %, 12–12 h light/dark cycle with easy and free access to water and food in accordance with the protocols of the National Committee for Research Ethics (IR.MUI.RESEARCH.REC.1397.405) [ 14 , 15 ].…”
Background and aim
Approximately, 2 million tonnes of pesticides are utilized annually worldwide. Phosalone (Pln), an organophosphorus pesticide, acts as an insecticide and acaricide to control pests of crops such as nuts, citrus fruits, pomegranates, stone fruits, grapes, potatoes, and artichokes. The purpose of this study was to evaluate the possible genotoxic effects following exposure to Pln in the cells derived from mouse red bone marrow.
Materials and methods
Sixty mice were divided into 6 groups including cyclophosphamide (40 mg/kg, IP) and Pln (6, 12, 20, and 40 mg/kg) exposure by gavage. After 1 and 5 days of exposure, animals were euthanized and the genotoxicity assays were done on bone marrow extracted cells.
Results
Comet assay shows a time and dose-dependent toxicity which further DNA degradation is observed after 5-day exposure (p < 0.05). Also, Pln significantly increased the MnPCE/PCE ratio after 12 and 20 mg/kg administration while no significant difference was reported between the doses of 6 and 40 mg/kg BW with the negative control group.
Conclusion
Our results suggested a serious concern about its potential effects on biological life and related disease inductions. However further studies need to confirm the exact mechanism of Pln genotoxicity and the cause of diverse response of its activity at 40 mg/kg. This study also showed that increasing the dose of Pln reduces the MnNCE/Total cells ratio, which may indicate the possibility of bone marrow suppression. All of the above results emphasize the need to seriously limit the use of this compound as an agricultural pesticide.
“…The current study was carried out on 60 Swiss albino male mice aged 6–8 weeks and weighing approximately 20–25 g, which were obtained from the animal house of faculty of Pharmacy at Isfahan University of Medical Sciences, Iran. The animals were kept in controlled conditions at a temperature of 20 ± 2 °C, humidity of about 50–60 %, 12–12 h light/dark cycle with easy and free access to water and food in accordance with the protocols of the National Committee for Research Ethics (IR.MUI.RESEARCH.REC.1397.405) [ 14 , 15 ].…”
Background and aim
Approximately, 2 million tonnes of pesticides are utilized annually worldwide. Phosalone (Pln), an organophosphorus pesticide, acts as an insecticide and acaricide to control pests of crops such as nuts, citrus fruits, pomegranates, stone fruits, grapes, potatoes, and artichokes. The purpose of this study was to evaluate the possible genotoxic effects following exposure to Pln in the cells derived from mouse red bone marrow.
Materials and methods
Sixty mice were divided into 6 groups including cyclophosphamide (40 mg/kg, IP) and Pln (6, 12, 20, and 40 mg/kg) exposure by gavage. After 1 and 5 days of exposure, animals were euthanized and the genotoxicity assays were done on bone marrow extracted cells.
Results
Comet assay shows a time and dose-dependent toxicity which further DNA degradation is observed after 5-day exposure (p < 0.05). Also, Pln significantly increased the MnPCE/PCE ratio after 12 and 20 mg/kg administration while no significant difference was reported between the doses of 6 and 40 mg/kg BW with the negative control group.
Conclusion
Our results suggested a serious concern about its potential effects on biological life and related disease inductions. However further studies need to confirm the exact mechanism of Pln genotoxicity and the cause of diverse response of its activity at 40 mg/kg. This study also showed that increasing the dose of Pln reduces the MnNCE/Total cells ratio, which may indicate the possibility of bone marrow suppression. All of the above results emphasize the need to seriously limit the use of this compound as an agricultural pesticide.
“…It has been suggested that miR-155-3p operates in the process of autoimmune demyelination with selective expression during EAE [22]. The results of recent studies based on the EAE model induced by cuprizone (a copper chelator molecule that affects oligodendrocytes) confirmed that decreasing expression of miR-155-3p can prevent microglia activation, myelin damage, and MS progression [90,91]. Analysis of miR-155 expression carried out on a mouse model allowed revealing the effect of the probiotic bacteria, Lactobacillus casei, on the recovery of demyelinated animals by regulating the immune response [92].…”
Multiple sclerosis (MS) is a chronic, immune-mediated disease and the leading cause of disability among young adults. MicroRNAs (miRNAs) are involved in the post-transcriptional regulation of gene expression. Of them, miR-155 is a crucial regulator of inflammation and plays a role in modulating the autoimmune response in MS. miR-155 is involved in blood–brain barrier (BBB) disruption via down-regulation of key junctional proteins under inflammatory conditions. It drives demyelination processes by contributing to, e.g., microglial activation, polarization of astrocytes, and down-regulation of CD47 protein and affecting crucial transcription factors. miR-155 has a huge impact on the development of neuropathic pain and indirectly influences a regulatory T (Treg) cell differentiation involved in the alleviation of pain hypersensitivity. This review also focused on neuropsychiatric symptoms appearing as a result of disease-associated stressors, brain atrophy, and pro-inflammatory factors. Recent studies revealed the role of miR-155 in regulating anxiety, stress, inflammation in the hippocampus, and treatment-resistant depression. Inhibition of miR-155 expression was demonstrated to be effective in preventing processes involved in the pathophysiology of MS. This review aimed to support the better understanding the great role of miR-155 dysregulation in various aspects of MS pathophysiology and highlight future perspectives for this molecule.
“…Treatment with the anti-malarial drug hydroxychloroquine saw attenuation of the MS phenotype as well as halving miR-155-3p expression [112]. Meanwhile, an independent study showed Apamin treatment to reduce miR-155-3p expression below that of the healthy control during the demyelination phase (figure 5 a ) [121]. Both treatments are known to target and inhibit the activity of microglial cells, possibly signifying that miR-155-3p plays a wider role in the CNS inflammatory landscape beyond that previously documented in astrocytes [120].…”
Section: The Immune Function Of Mir-155-3pmentioning
confidence: 99%
“…Figure 5Inducers and targets of miR-155-3p in immunity. ( a ) Inducers, targets and phenotypic effects of miR-155-3p in specific cellular or pathological contexts, including dendritic cells [107], trophoblasts [108], macrophages [114,119], astrocytes [120], CD4+ T cells [105], EAE and multiple sclerosis [112,121]. ( b ) Graphic representation of positive and negative inflammatory feedback loops of miR-155-3p within the NF-κB pathway.…”
Section: The Immune Function Of Mir-155-3pmentioning
MicroRNAs (miRNAs) are key players in gene regulation that target specific mRNAs for degradation or translational repression. Each miRNA is synthesized as a miRNA duplex comprising two strands (5p and 3p). However, only one of the two strands becomes active and is selectively incorporated into the RNA-induced silencing complex in a process known as miRNA strand selection. Recently, significant progress has been made in understanding the factors and processes involved in strand selection. Here, we explore the selection and functionality of the miRNA star strand (either 5p or 3p), which is generally present in the cell at low levels compared to its partner strand and, historically, has been thought to possess no biological activity. We also highlight the concepts of miRNA arm switching and miRNA isomerism. Finally, we offer insights into the impact of aberrant strand selection on immunity and cancer. Leading us through this journey is miR-155, a well-established regulator of immunity and cancer, and the increasing evidence that its 3p strand plays a role in these arenas. Interestingly, the miR-155-5p/-3p ratio appears to vary dependent on the timing of the immune response, and the 3p strand seems to play a regulatory role upon its partner 5p strand.
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