10 research outputs found

    Effects of Chamomile Essential Oil on Granulocyte Count In Patients with Neutropenia

    Get PDF
    Introduction Neutropenia is an abnormality in neutrophil count which lessens to lower than 1500 / microL (<1.5×109/L). Early recognition and treatment are needed in neutropenia cases. Matricaria chamomilla (chamomile) belongs to Asteracea family which often is referred as "star among medicinal species". Recently, valuable effects of chamomile in multitherapy, cosmetics and nutrition has been published in several papers. The phytochemical analysis exhibited flavonoids, essential oils, cumarins and sesquiterpene lactones derivatives like matricin and chamazulene in the plant. The aim of this research wasevaluation of chamomile essential oil on granulocyte count in patients with neutropenia. Methods and Results Essential oil of chamomile was collected consecutively via Clevenger method.  85 people were participated in the clinical trial and divided into three groups. 15 healthy people as control group received chamomile drop, 35 neutropenia patients induced by chemotherapy received chamomile drop as treatment group and 35 neutropenia patients induced by chemotherapy did not receive the drop as non-treated group. Blood sampling was done at the time of the admission and every other day for 10 consecutive days after chamomile drop consumption. Granulocytes, polymorphonuclear cells (PMNs) and white blood cells (WBC) were counted after every sampling. The average of WBC, PMNs and granulocytes numbers were significantly raised in control and treatment group with P<0.05 90±11/ 3520±611, 1.14±0.83/ 17.37±22.8 and 150±0.07/ 1537±305, respectively. In non-treated group the WBC, PMNs and granulocyte were 40±72, 7.91±22.96 and 190±48, respectively.        ConclusionConsumption of chamomile drop significantly increased the level of WBC, PMNs and granulocyte in control and treatment groups in comparison to non-treated group. As the result, chamomile essential oil could be considered as an adjuvant in neutropenia or other immune system deficiencies

    Cellular and molecular mechanisms of sulfur mustard toxicity on spermatozoa and male fertility

    Get PDF
    Sulfur mustard (SM) is a toxic compound that can target human spermatozoa. SM induces a wide variety of pathological effects in human reproductive organs, including sexual hormone disturbance, testicular atrophy, impaired spermatogenesis, poor sperm quality, defects in embryo development, childhood physical abnormalities, and severe fertility problems. However, the molecular and cellular mechanisms of SM action on male reproductive health and human sperm function are unclear. Excessive production of reactive oxygen species and the resulting oxidative stress is likely a significant mechanism of SM action, and could be associated with sperm DNA damage, membrane lipid peroxidation, reduced membrane fluidity, mitochondrial deficiency, apoptosis, and poor sperm quality. In this review, we aim to discuss the cellular and molecular mechanisms of SM action on sperm and reproductive health, the significance of OS, and the mechanisms through which SM enhances the infertility rate among SM-exposed individuals

    Screening of a clinically and biochemically diagnosed SOD patient using exome sequencing: A case report with a mutations/variations analysis approach

    Get PDF
    Background: Sulfite oxidase deficiency (SOD) is a rare neurometabolic inherited disorder causing severe delay in developmental stages and premature death. The disease follows an autosomal recessive pattern of inheritance and causes deficiency in the activity of sulfite oxidase, an enzyme that normally catalyzes conversion of sulfite to sulfate. Aim of the study: SOD is an underdiagnosed disorder and its diagnosis can be difficult in young infants as early clinical features and neuroimaging changes may imitate some common diseases. Since the prognosis of the disease is poor, using exome sequencing as a powerful and efficient strategy for identifying the genes underlying rare mendelian disorders can provide important knowledge about early diagnosis, disease mechanisms, biological pathways, and potential therapeutic targets. Patients and methods: In this study, a case who was a newborn infant boy with suspected SOD and his healthy parents were recruited for exome sequencing. The first laboratory reports of the patient were positive urine sulfite, elevated urinary thiosulfate, and high levels of plasma lactate and pyruvate. The patient also presented some symptoms such as intractable seizures, abnormal tone, feeding difficulties, profound mental retardation, abnormal respiratory drive, aspiration pneumonia, microcephaly, and dislocated ocular lenses. The genomic DNA of the patient and his parents was extracted from peripheral blood lymphocytes as targets for exome sequencing, performed by Axeq Technologies (Amsterdam, the Netherlands). Results: The results showed no single predominate mutation in the SUOX gene as one of the candidate genes involved in the catabolism of sulfur-containing amino acids. The same results obtained in the molybdenum cofactor biosynthetic genes (MOCS1, MOCS2, and GEPH genes). Instead, the results revealed that causal variations are present in genes underlying in different biochemical pathways among which the sulfur metabolism, signaling and signal transduction, and transcription pathways are of higher importance. Conclusion: In this study, several classes of genes were introduced as candidate genes involved in SOD. However, further studies are necessary to examine the reported genes in more details on how these genes may relate to each other and contribute to the pathology of SOD disease

    Role of oxidative stress and antioxidant therapy in acute and chronic phases of sulfur mustard injuries: a review

    No full text
    Sulfur mustard (SM) is a chemical compound that preferentially targets ocular, cutaneous and pulmonary tissues. Although pathologic effect of SM has been extensively considered, molecular and cellular mechanism of its toxicity, especially at the chronic phase of injury is not well-understood. Excessive production of reactive oxygen species (ROS) and oxidative stress (OS) appears to be involved in SM-induced injuries. SM may trigger several molecular and cellular pathways linked to OS and inflammation that can subsequently result in cell death and apoptosis. At the acute phase of injury, SM can enhance ROS production and OS by reducing the activity of antioxidants, depletion of intercellular glutathione (GSH), decreasing the productivity of GSH-dependent antioxidants, mitochondrial deficiency, accumulation of leukocytes and pro-inflammatory cytokines. Overexpression of ROS producing enzymes and down-regulation of antioxidant enzymes are probably the major events by which SM leads to OS at the chronic phase of injury. Therefore, antioxidant therapy with potent antioxidants such as N-acetylcysteine and curcumin may be helpful to mitigate SM-induced OS damages. This review aims to discuss the proposed cellular and molecular mechanisms of acute and delayed SM toxicity, the importance of OS and mechanisms by which SM increases OS either at the acute or chronic phases of injuries along with research on antioxidant therapy as a suitable antidot

    A review on proteomics analysis to reveal biological pathways and predictive proteins in sulfur mustard exposed patients: roles of inflammation and oxidative stress

    No full text
    Sulfur mustard (SM) is a mutagenic compound that targets various organs. Although it causes a wide range of abnormalities, cellular and molecular mechanisms of its action are not-well-understood. Oxidation of DNA, proteins, lipids, as well as depletion of cellular nicotinamide adenine dinucleotide (NAD), antioxidants and increase of intracellular calcium are the hypothesized mechanisms of its action at the acute phase of injury. In this review, the proteome analysis of SM toxicity has been considered. We selected articles that considered proteomics analysis of SM toxicity with two-dimensional gel electrophoresis (2DE) followed by mass spectrometry. Our search yielded nine related articles, four original in vitro and five human studies. The results of these studies have revealed a change in expression pattern of various proteins such as haptoglobin, amyloid A1, surfactant proteins, S100 proteins, apolipoprotein, Vit D binding protein, transferrin, alpha 1 antitrypsin, protein disulfide isomerase and antioxidant enzymes in patients who were exposed to SM about 30 years ago. Most of these proteins are up- or down-regulated in response to excessive production of reactive oxygen species (ROS) and oxidative stress (OS). There is a tight link between the expression pattern of these proteins with accumulation of leukocytes, inflammatory conditions, antioxidant depletion, mitochondrial deficiency, as well as increased expression or activity of several proteases such as caspases and matrix metalloproteinases (MMPs). Therefore, excessive production of ROS and OS along with chronic inflammatory may be the long-term toxic effects of SM following acute exposure
    corecore