rss_2.0Interdisciplinary Toxicology FeedSciendo RSS Feed for Interdisciplinary Toxicology Toxicology 's Cover of tramadol dependence on male sexual dysfunction<abstract><title style='display:none'>Abstract</title><p>Tramadol dependence became an increasing and alarming problem in the Egyptian community. Wide availability of tramadol as a pain killer and its role in the treatment of premature ejaculation may be the most apparent causes of increased magnitude of the problem among youth who believe that tramadol has a positive impact on their sexual functions. This study aimed to explore the real impact of chronic tramadol administration on sexual functions in males dependent on tramadol. The study was carried on 80 subjects (50 subjects were tramadol dependent group and 30 subjects represented the control group). Personal, family and past histories were obtained from all the participants in addition to the toxicological history from tramadol dependent group. Urine screening for tramadol was done for all cases of history of tramadol dependence then confirmation by HPLC technique to measure tramadol blood level was done. Both groups were investigated for serum testosterone and prolactin level. Curiosity (22%) and treatment of premature ejaculation (20%) were the main motives for dependence. Erectile dysfunction and decreased libido occurred in 44% and 48% of tramadol dependent group respectively. Significant increase in erectile dysfunction and decreased libido was noted as the duration of dependence increased. Additionally, significant decrease in serum testosterone level and increase in serum prolactin level as tramadol daily dose and duration increased was found. In conclusion, men who take tramadol for premature ejaculation or any other purpose must know that they are very susceptible to many sexual dysfunctions.</p></abstract>ARTICLE2020-04-30T00:00:00.000+00:00Mechanism of protection of rat hepatocytes from acetaminophen-induced cellular damage by ethanol extract of<abstract><title style='display:none'>Abstract</title><p>The aim of this study is to evaluate the protective effect of ethanol extract of <italic>Aerva lanata</italic> (EEAL) in preventing acetaminophen induced liver toxicity. EEAL was prepared and its hepatoprotective effect was studied in both isolated primary hepatocytes <italic>in vitro</italic> and in Sprague Dawley rats <italic>in vivo</italic>. For <italic>in vivo</italic> studies, the animals were grouped as Group I – Control; Group II – ACN (2 g/kg b.w.); Group III – EEAL (50 mg/kg b.w.) + ACN (2 g/kg b.w.), Group IV – EEAL (100 mg/kg b.w.) + ACN (2 g/kg b.w.). Extracellular activities of the enzymes liver aminotransferease (GOT, GPT), alkaline phosphatase (ALP) and lactate dehydrogenase (LDH) in isolated hepatocytes and rat plasma were studied colorimetrically. Expression of GST, Nrf2, COX 1 &amp; COX2 genes in rat liver were evaluated by RT-PCR. The results showed that ACN induced down-regulation of Nrf2 and upregulation of GST gene expression, which were modulated by EEAL treatment. GOT, GPT, ALP and LDH levels were found to be lowered in both hepatocyte culture media and plasma following EEAL treatment. In addition, the medium GOT and GPT levels were diminished following EEAL treatment only. Moreover, only ALP and LDH in serum appeared to be at normal level following EEAL treatment, whereas GOT and GPT showed levels lower than control. ACN treatment increased the expression of pro-inflammatory COX 1 and COX 2 genes and the levels of these genes were reduced by EEAL treatment. EEAL pre-treated rats exposed to ACN were found to retain normal hepatic structure compared to ACN alone treated rats. From these results it can be concluded that ethanol extract of <italic>A. lanata</italic> possesses both anti-inflammatory and hepatoprotective activity.</p></abstract>ARTICLE2020-04-30T00:00:00.000+00:00The effect of venlafaxine on blood pressure and ECG in rats fed with high-fat-fructose diet<abstract><title style='display:none'>Abstract</title><p>Metabolic syndrome represents one of the major health, social and economic issues nowadays, and affects more than 25% people worldwide. Being a multifactorial health problem, metabolic syndrome clusters various features, such as obesity, dyslipidemia, hyperglycemia and hypertension. Each of these disturbances represents a risk factor for developing cardiovascular disease. Moreover, patients with metabolic syndrome are more likely to suffer from depression, thus treatment with antidepressants (<italic>e.g.</italic> venlafaxine) is often neccessary. However, many of the antidepressants themselves may contribute to worsening or even development of the metabolic syndrome, thus creating a “vicious circle”. The aim of this work was to investigate on the animal model of metabolic syndrome, i.e. on hypertriacylglycerolemic rats fed high-fat-fructose diet (HFFD): 1) the effect of a change in diet from HFFD to a standard diet (SD) and the effect of venlafaxine treatment, 2) during HFFD, 3) as well as during a changed diet to SD. We focused on biometric parameters, blood pressure and selected ECG parameters. We observed the reversibility of the present metabolic and cardiovascular changes by switching the HFFD to SD in the last 3 weeks of the experiment. Switch to the standard diet led to decrease of body weight, even in the presence of venlafaxine. Administration of venlafaxine caused the decrease of heart weight/body weight index in rats fed with HFFD compared to the untreated group fed with HFFD for 8 weeks. Blood pressure, which was increased in the HFFD group showed a tendency to decrease to control values after switching to the standard diet. Administration of venlafaxine led to significant increase in all parameters of blood pressure when rats were fed with HFFD throughout the whole experiment. In untreated rats fed with HFFD for 8 weeks, we observed a shorter PQ interval and prolonged QRS complex as well as QTc interval compared to untreated rats with diet switched to SD. This effect was potentiated by venlafaxine administered not only during HFFD but even after switch to SD. Our results point to the fact that metabolic syndrome is clearly affecting the function of the cardiovascular system by modifying blood pressure and electrical activity of the heart. Moreover, administration of venlafaxine may lead to worsening of the observed changes, especially in the presence of high-fat-fructose diet.</p></abstract>ARTICLE2020-04-30T00:00:00.000+00:00Biochemical and histopathological effects of sub-acute exposure of albino rats to fumigants – dichlorvos and cypermethrin<abstract><title style='display:none'>Abstract</title><p>Cypermethrin (CYP) is one of the most common active ingredients in most insecticides, mosquito coils and powder used in Nigeria. dichlorvos (DDVP) is the most indiscriminately used fumigant in most rural and sub-urban areas in Nigeria. These fumigants can easily be accessed without proper method of usage thus exposing the population to their toxic effects. As a result, this study was initiated to determine the effects of sub-acute exposure of CYP and DDVP on some biochemical and histopathological parameters of albino rats. In this study, forty (40) albino rats of 10 groups of 4 rats per group, with one group serving as control, were exposed to these fumigants in a poorly ventilated area for 4hours per day over 2, 4 and 6 weeks. The results showed observable changes in liver enzyme activities (<italic>p</italic>&lt;0.05) in groups exposed to DDVP for 2, 4 and 6 weeks. The groups exposed to CYP showed mild changes in liver enzyme activities when compared with the DDVP groups. Increase in activity of the liver enzymes was also observed in the groups exposed to a mixture of DDVP+CYP for 2, 4 and 6 weeks. The urea, creatinine and electrolytes levels in all the groups exposed to DDVP, CYP and DDVP+CYP for 2, 4 and 6weeks were significantly (<italic>p</italic>&lt;0.05) increased. Also WBC and platelets in all the groups exposed to DDVP and CYP recorded significant changes. The histology report of the lungs and liver showed moderate lymphocytic infiltration and hepatocytic steatosis which progressed with duration of exposure to the fumigants, while the kidneys showed no remarkable changes. The results of this study suggest that DDVP and CYP have relative toxic effects in the exposed animals and should be used with caution to avoid human exposure to their visible toxicities.</p></abstract>ARTICLE2020-04-30T00:00:00.000+00:00Melamine migration measurement through spectrophotometry device and the effect of time and tableware type on it<abstract><title style='display:none'>Abstract</title><p>Melamine is an organic-based chemical material widely used in the production of tableware. Given the adverse effects of melamine on human health, melamine tableware can be a source for its introduction into the human body. The aim of this study was to use a simple method for monitoring the rate of melamine migration from the tableware to food and the effect of time and tableware on this migration. To measure the migration, spectrophotometry was used. The limit of detection (LOD) of the method was 0.2 (μg/ml), which is functional for measuring the rate of migration. The investigation of sample migration of melamine tableware revealed that migration has occurred across all samples. The rate of migration in all samples was less than the standard level of the European Union (30 μg/ml). Statistical analysis indicated that time is an important factor in melamine migration, which significantly increased (<italic>p</italic>&lt;0.05) in 93% of cases with lengthening the contact time from 30 minutes to 90 minutes. The type of tableware (new or old) and production conditions (standard or non-standard) were found to significantly affect (<italic>p</italic>&lt;0.001) the rate of migration. Statistical analysis of the results suggested that old tableware increased melamine migration in 41% of cases (<italic>p</italic>&lt;0.05). Non-standard tableware significantly (<italic>p</italic>&lt;0.001) increased the rate of migration and thus the effect of non-standard production on melamine tableware was more significant than the age of the tableware.</p></abstract>ARTICLE2020-04-30T00:00:00.000+00:00The hepatoprotective and antioxidative effect of saffron stigma alcoholic extract against vincristine sulfate induced toxicity in rats<abstract><title style='display:none'>Abstract</title><p>Vincristine (VCR) is an important anti-cancer drug, which is highly toxic for the liver. This study aimed at evaluating the protective effect of alcoholic extract of saffron stigma against vincristine hepatotoxicity in the rat. A total number of 50 rats were randomly divided into 10 groups, including controls, rats receiving 0.25 mg/kg (A group), 0.5 mg/kg (B group), 0.75 mg/kg (C group) VCR, 0.25 mg/kg VCR + 0.5 mg/kg saffron (D group), 0.5 mg/kg VCR + 0.5 mg/kg saffron (E group), 0.75 mg/kg VCR + 0.5 mg/kg saffron (F group), 0.25 mg/kg VCR + 1mg/kg saffron (G group), 0.5 mg/kg VCR + 1 mg/kg saffron (H group), and 0.75 mg/kg VCR + 1 mg/kg saffron (I group) groups. Serum level of liver enzymes, including aspartate transaminase (AST), alanine transaminase (ALT), alkaline phosphatase (ALP), and bilirubin were measured using specific kits at the end of the experimental period. Serum total antioxidant capacity (TAC) and malondialdehyde (MDA) values were measured using ferric reducing antioxidant of power (FRAP) and thiobarbituric acid reaction (TBAR) methods, respectively. Administration of VCR, especially at the concentration of 0.75mg/kg, caused severe hepatic injury with significant increase in the levels of AST (582.0±39.45 UI), ALT (124.0±5.92 UI), ALP (939.8±89.8 UI) enzymes and bilirubin (0.17±0.008). VCR administration also significantly increased the serum MDA level (0.49±0.021 nmol/ml), while TAC value was declined significantly (241.27±18.27 μmol/l). These effects were dose-dependent. Treatment with saffron extract decreased the activity of liver enzymes and MDA values in hepatotoxic rats with a significant enhancement in serum TAC content. These effects were notable for rats that received 1mg/kg plant extract. Administration of saffron, especially at higher concentration, can reduce VCR-induced hepatotoxicity, antioxidant depletion and lipid peroxidation, presumably due to its antioxidative properties.</p></abstract>ARTICLE2020-04-30T00:00:00.000+00:00The present approaches to the development of prophylactic and therapeutic antidotes against nerve agents<abstract xml:lang="en"><title style='display:none'>The present approaches to the development of prophylactic and therapeutic antidotes against nerve agents</title><p>Nerve agents belong to highly toxic organophosphorus compounds misused as chemical warfare agents for military as well as terroristic purposes. Basic mechanism of action of nerve agents is based on acetylcholinesterase (AChE, EC inhibition and subsequent accumulation of neuromediator acetylcholine at the cholinergic synapses, either peripheral or central leading to cholinergic hyperstimulation and development of symptoms of poisoning, followed by metabolic dysbalance and death without effective prophylaxis/treatment. The antidotal treatment of acute poisonings with nerve agents still represents a serious problem and, therefore, we are searching how to satisfactorily protect people against acute toxicity of nerve agents. There are two approaches how to improve the medical protection against nerve agents:</p><p>to increase the resistance of nerve agent-exposed organism and the efficacy of post-exposure antidotal treatment by pharmacological prophylaxis</p><p>the development of new, more effective antidotes, expecially AChE reactivators, to achieve the satisfactorily effective antidotal treatment of acute poisonings with nerve agents.</p></abstract>ARTICLE2010-11-01T00:00:00.000+00:00Trends in the study of genetic susceptibility<abstract xml:lang="en"><title style='display:none'>Trends in the study of genetic susceptibility</title><p>Genotoxicology investigates the molecular basis of cellular responses to DNA damage. During more than three decades of genetic toxicology testing, a large number of tests with varying sensitivity and specificity have been developed.</p><p>These genotoxicity tests can predict:</p><p>the likelihood of a substance to be a (rodent) carcinogen,</p><p>the mechanism of carcinogenic activity of different substances,</p><p>if the results of genotoxicity studies only predict carcinogenicity or they are a distinct hazard endpoint (Nohynek, 2005).</p><p>The current genetic toxicity testing batteries represent:</p><p>Ames test which is a component of all genetic testing batteries.</p><p>A mammalian cell mutagenicity assay which should confirm or complete the Ames test.</p><p>Chromosomal aberrations tests which are based on a different endpoint than gene mutations.</p><p>Positive <italic>in vitro</italic> results need to be confirmed by in vivo tests; results from test batteries have higher predictive value than results of a single test (Nohynek, 2005).</p></abstract>ARTICLE2010-11-01T00:00:00.000+00:00Enzyme systems of detoxication — overview of recent approaches<abstract xml:lang="en"><title style='display:none'>Enzyme systems of detoxication — overview of recent approaches</title><p>The most important enzymes of detoxication are cytochromes P450 of Phase I and UDPglucuronosyltransferases of Phase II of drug metabolism. The conventional division of drug, or xenobiotic, metabolism to two phases has survived almost fifty years and although not perfect, still is rather informative and practical. The recent addition of the next, third phase to the first two (Phase I as yielding a molecule with free functional groups ready for conjugation with another molecule or its part in Phase II) stressed the importance of drug transport across the membranes even if it is not a pure metabolic process (i.e. a process changing the polarity and structure of a compound).</p></abstract>ARTICLE2010-11-01T00:00:00.000+00:00Important issues in developmental toxicity testing<abstract xml:lang="en"><title style='display:none'>Important issues in developmental toxicity testing</title><p>Studies of individual development and its possible deterioration have been the concern since the 19th century, when Etienne Geoffroy de Saint-Hilaire (1772-1844) with his pioneer experiments opened the door for future experimental teratologists. Later scientists, focused on environmental agents which can alter embryonic and fetal development, such hyperthermia, malnutrition, pharmaceuticals, microbial toxins etc. Although the history of teratology involves many notable scientists, it has gained prominence after the big thalidomide tragedy in 1961. Principles of teratology were proposed later by James Wilson in his monograph <italic>Environment and Birth Defects</italic> (Wilson, 1973).</p></abstract>ARTICLE2010-11-01T00:00:00.000+00:00Acute toxicity of binary mixtures: alternative methods, QSAR and mechanisms<abstract xml:lang="en"><title style='display:none'>Acute toxicity of binary mixtures: alternative methods, QSAR and mechanisms</title><p>Committee accepted the program of chemical safety in October 2003 called REACH, meaning "Registration, Evaluation, Authorization of Chemicals". The protection of health of nature, including human beings, against harmful effects of chemicals is a goal of these programs. The development and research on new chemicals can become, however, cheaper than their testing and registration. The aim of effort of the present is, thus, to develop and to use alternative methods of testing toxic and adverse effects of chemicals, which would be cheaper and more informative than traditional tests with experimental animals.</p></abstract>ARTICLE2010-11-01T00:00:00.000+00:00Developmental origin of chronic diseases: toxicological implication<abstract xml:lang="en"><title style='display:none'>Developmental origin of chronic diseases: toxicological implication</title><p>Human epidemiological and experimental animal studies show that suboptimal environments in fetal and neonatal life exerts a profound influence on physiological function and risk of disease in adult life. The molecular, cellular, metabolic, endocrine and physiological adaptations to intrauterine nutritional conditions result in permanent alterations of cellular proliferation and differentiation of tissues and organ systems, which in turn can manifest by pathological consequences or increased vulnerability to chronic diseases in adulthood. Intrauterine growth restriction (IUGR) due to intrauterine development derangements is considered the important factor in development of such diseases as essential hypertension, diabetes mellitus, ischemic diseases of the heart, osteoporosis, respiratory, neuropsychiatric and immune system diseases.</p><p>An early life exposures to dietary and environmental exposures can have a important effect on epigenetic code, resulting in diseases developed later in life. The concept of the "developmental programming" and Developmental Origins of Adult Diseases (DOHaD) has become well accepted because of the compelling animal studies that have precisely defined the outcomes of specific exposures. The environmental pollullutants and other chemical toxicants may influence crucial cellular functions during critical periods of fetal development and permanently alter the structure or function of specific organ systems. Developmental epigenetics is believed to establish "adaptive" phenotypes to meet the demands of the later-life environment. Resulting phenotypes that match predicted later-life demands will promote health, while a high degree of mismatch will impede adaptability to later-life challenges and elevate disease risk. The rapid introduction of synthetic chemicals, environmental pollutants and medical interventions, may result in conflict with the programmed adaptive changes made during early development, and explain the alarming increases in some diseases.</p></abstract>ARTICLE2010-11-01T00:00:00.000+00:00Contribution of biotransformation enzymes to the development of renal injury and urothelial cancer caused by aristolochic acid: urgent questions, difficult answers<abstract xml:lang="en"><title style='display:none'>Contribution of biotransformation enzymes to the development of renal injury and urothelial cancer caused by aristolochic acid: urgent questions, difficult answers</title><p>Ingestion of aristolochic acid (AA) is associated with the development of aristolochic acid nephropathy, which is characterized by chronic renal failure, tubulointerstitial fibrosis and urothelial cancer. AA may also cause a similar type of kidney fibrosis with malignant transformation of the urothelium, the Balkan endemic nephropathy. Understanding which enzymes are involved in AA activation and/or detoxication is important in the assessment of a susceptibility to this carcinogen. The most important human enzymes activating AA by simple nitroreduction <italic>in vitro</italic> are hepatic and renal cytosolic NAD(P)H:quinone oxidoreductase, hepatic microsomal cytochrome P450 1A2 and renal microsomal NADPH:cytcohrome P450 reductase, besides cyclooxygenase, which is highly expressed in urothelial tissue. Despite extensive research, contribution of most of these enzymes to the development of these diseases is still unknown. Hepatic cytochromes P450 were found to detoxicate AA in mice, and thereby protect the kidney from injury. However, which of cytochromes P450 are the most important in this process both in animal models and in humans have not been entirely resolved as yet. In addition, the relative contribution of enzymes found to activate AA to species responsible for induction of urothelial cancer in humans remains still to be resolved.</p></abstract>ARTICLE2010-11-01T00:00:00.000+00:00Acute and delayed sulfur mustard toxicity; novel mechanisms and future studies<abstract xml:lang="en"><title style='display:none'>Acute and delayed sulfur mustard toxicity; novel mechanisms and future studies</title><p>Sulfur mustard (SM), also known as mustard gas, has been the most widely used chemical weapon. The toxicity of SM as an incapacitating agent is of much greater importance than its ability to cause lethality. Acute toxicity of SM is related to reactive oxygen and nitrogen species, DNA damage, poly(ADP-ribose) polymerase activation and energy depletion within the affected cell. Therefore melatonin shows beneficial effects against acute SM toxicity in a variety of manner. It scavenges most of the oxygen- and nitrogen-based reactants, inhibits inducible nitric oxide synthase, repairs DNA damage and restores cellular energy depletion. The delayed toxicity of SM however, currently has no mechanistic explanation. We propose that epigenetic aberrations may be responsible for delayed detrimental effects of mustard poisoning. Epigenetic refers to the study of changes that influence the phenotype without causing alteration of the genotype. It involves changes in the properties of a cell that are inherited but do not involve a change in DNA sequence. It is now known that in addition to genetic mutations, epimutations can also involve in the pathogenesis of a variety of human diseases. Several actions of melatonin are now delineated by epigenetic actions including modulation of histone acetylation and DNA methylation. Future studies are warranted to clarify whether epigenetic mechanisms are involved in pathogenesis of delayed sulfur mustard toxicity and melatonin alleviates delayed toxicity of this warfare agent.</p></abstract>ARTICLE2010-11-01T00:00:00.000+00:00Assessment of the time-dependent dermatotoxicity of mechlorethamine using the mouse ear vesicant model<p>Mechlorethamine (HN2) is an alkylating agent and sulfur mustard gas mimetic which is also used in anticancer therapy. HN2 is associated with skin inflammation and blistering which can lead to secondary infections. The purpose of the present study was to investigate the time-dependent dermatotoxicity of HN2 using the mouse ear vesicant model (MEVM). To this end, our operational definition of dermatotoxicity included tissue responses to HN2 consistent with an increase in the wet weights of mouse ear punch biopsies, an increase in the morphometric thickness of H&amp;E stained ear sections and histopathologic observations including tissue edema, inflammatory cell infiltration and vesication. The ears of male Swiss Webster mice were topically exposed to a single dose of HN2 (0.5 µmol/ear) or DMSO vehicle (5 µl/ear) or left untreated (naive). Mice were then euthanized at 15 min, 1, 2, 4, 8 or 24 hr following HN2 exposure. Compared to control ears, mouse ears exposed to HN2 at all time points showed an increase in wet weights, morphometric thickness, edema, inflammatory cell infiltration and signs of vesication. The incidence in tissue vesication sharply increased between 4 and 8 hr after exposure, revealing that tissue vesication is well established by 8 hr and remains elevated at 24 hr after exposure. It is noteworthy that, compared to control ears, mouse ears treated with DMSO vehicle alone also exhibited an increase in wet weights and morphometric thickness at 15 min, 1, 2 and 4 hr following treatment; however, these vehicle effects begin to subside after 4 hr. The results obtained here using the MEVM provide a more holistic understanding of the kinetics of vesication, and indicate that time points earlier than 24 hr may prove useful not only for investigating the complex mechanisms involved in vesication but also for assessing the effects of vesicant countermeasures.</p>ARTICLE2019-10-18T00:00:00.000+00:00Novel pentacyclic triterpene isolated from seeds of ameliorates diabetes in streptozotocin induced diabetic rats<p>The present research was carried out to study the effect of 2β-hydroxybetulinic acid 3β-oleiate (HBAO), a novel compound isolated from the seeds of <italic>Euryale ferox salisb.</italic> on glycemic control, antioxidant status and histopathological morphological alterations in the liver, pancreas, kidney and heart in streptozotocin induced type-2 diabetes in rats. HBAO was isolated from the seeds of <italic>Euryale ferox salisb.</italic> according to Lee. Isolation of the active principle HBAO was performed for the first time. To date there are no reports on the isolation and evaluation of 2β-hydroxybetulinic acid 3β-oleiate (HBAO) from <italic>Euryale ferox salisb.</italic> Assessment of different biochemical parameters like the effect of HBAO on glycemic control, plasma insulin, glycosylated hemoglobin, hepatic glucose-6-phosphate dehydrogenase, glucose-6-phosphatase and fructose-1-6-biphosphatase, hepatic hexokinase, lipid profile, antioxidant marker and histopathology of pancreas, liver and kidney examination was done at the end of the experimentation, i.e. on day 45. HBAO exhibited remarkable improvement in glycemic control, lipid levels, plasma insulin, glycogenic liver enzymes and antioxidant activity in diabetic rats, along with progressive enhancement of distortive histopathological morphology of liver, pancreas and kidney. The results strongly suggest that HBAO could be a potential therapeutic agent in diabetes.</p>ARTICLE2019-10-18T00:00:00.000+00:00Impact of quercetin on tight junctional proteins and BDNF signaling molecules in hippocampus of PCBs-exposed rats<p>Polychlorinated biphenyls (PCBs) consist of a range of toxic substances which are directly proportional to carcinogenesis and tumor-promoting factors as well as having neurotoxic properties. Reactive oxygen species, which are produced from PCBs, alter blood–brain barrier (BBB) integrity, which is paralleled by cytoskeletal rearrangements and redistribution and disappearance of tight junction proteins (TJPs) like claudin-5 and occludin. Brain-derived neurotrophic factor (BDNF), plays an important role in the maintenance, survival of neurons and synaptic plasticity. It is predominant in the hippocampal areas vital to learning, memory and higher thinking. Quercetin, a flavonoid, had drawn attention to its neurodefensive property. The study is to assess the role of quercetin on serum PCB, estradiol and testosterone levels and mRNA expressions of estrogen receptor α and β, TJPs and BDNF signaling molecules on the hippocampus of PCBs-exposed rats. Rats were divided into 4 groups of 6 each. Group I rats were intraperitoneally (i.p.) administered corn oil (vehicle). Group II received quercetin 50 mg/kg/bwt (gavage). Group III received PCBs (Aroclor 1254) at 2 mg/kg bwt (i.p). Group IV received quercetin 50 mg/kg bwt (gavage) simultaneously with PCBs 2 mg/kg bwt (i.p.). The treatment was given daily for 30 days. The rats were euthanized 24 h after the experimental period. Blood was collected for quantification of serum PCBs estradiol and testosterone. The hippocampus was dissected and processed for PCR and Western blot; serum PCB was observed in PCB treated animals, simultaneously quercetin treated animals showed PCB metabolites. Serum testosterone and estradiol were decreased after PCB exposure. Quercetin supplementation brought back normal levels. mRNA expressions of estrogen α and β were decreased in the hippocampus of PCB treated rats. TJPS and BDNF signalling molecules were decreased in hippocampus of PCB treated rats. Quercetin supplementation retrieved all the parameters. Quercetin alone treated animals showed no alteration. Thus in PCB caused neurotoxicity, quercetin protects and prevents neuronal damage in the hippocampus.</p>ARTICLE2019-10-18T00:00:00.000+00:00Medicinal plants and natural products can play a significant role in mitigation of mercury toxicity<p>Mercury is a heavy metal of considerable toxicity. Scientific literature reveals various plants and plant derived natural products, <italic>i.e.</italic>, phytochemicals, which can alleviate experimentally induced mercury toxicity in animals. The present review attempts to collate those experimental studies on medicinal plants and phytochemicals with ameliorative effects on mercury toxicity. A literature survey was carried out by using Google, Scholar Google, Scopus and Pub-Med. Only the scientific journal articles found in the internet for the last two decades (1998–2018) were considered. Minerals and semi-synthetic or synthetic analogs of natural products were excluded. The literature survey revealed that in pre-clinical studies 27 medicinal plants and 27 natural products exhibited significant mitigation from mercury toxicity in experimental animals. Clinical investigations were not found in the literature. Admissible research in this area could lead to development of a potentially effective agent from the plant kingdom for clinical management of mercury toxicity in humans.</p>ARTICLE2019-10-18T00:00:00.000+00:00Measurement of melamine migration from melamine-ware products by designed HPLC method and the effect of food-type on the level of migration<p>Melamine-ware is widely used around the world. There is a public health concern as regards the safety of melamine when exposed to food. This study was carried out to measure the level of melamine migration in melamine-ware products by HPLC method and the effect of food-type on the level of melamine migration. In food control laboratories in Iran, there is no common method to measure and monitor melamine migration, hence a method using HPLC technique was adopted and validated to solve this problem. The validation results showed the reliability with 94.9% accuracy and 95.3% precision. Furthermore, the limit of detection (LOD) and quantification (LOQ) were 0.145 and 0.435 µg/ml, which for a new method were within acceptable ranges. Melamine migrations from 4 most available melamine wares were measured. Distilled water, 3% acetic acid and 15% ethanol were used as food simulant at 30 °C for 90 min. Although melamine migration occurred in all samples and acidic conditions had a significant effect, the values were not higher than the European standard (30 µg/ml). The study revealed that the HPLC method was valid and could be applied and developed to measure melamine migration. However, precautions should be considered while choosing melamine-ware utensil as long-term exposure to this substance has a negative effect on health, especially on the kidneys.</p>ARTICLE2019-10-18T00:00:00.000+00:00Zika virus infection from a newborn point of view. TORCH or TORZiCH?<p>Zika virus (ZIKV) belongs to the group of viruses called arboviruses. Congenital Zika syndrome is a new disease with infectious teratogenic aetiology. The clinical symptoms are divided into morphological and functional. Most severe complication is the foetal brain disruption sequence that includes severe microcephaly, anomalies of the eyes and congenital contractions of joints. The aim of this paper was to review available facts about Zika virus infection from a newborn point of view in a form of the summary of all important information. Zika virus infection is a problem of past, present and future. Epidemics may occur because of global climate changes, also in countries where natural conditions for life of mosquitos are not present. This clearly indicates the need to continue developing of vaccines and specific antiviral drugs. Until this happens, we must adhere individual preventive measures. Zika virus has proven to us how it can affect the health of adults and neonates but also thinking of healthy people. Newborns with microcephaly on the front pages of the media caused in 2015 panic and fear around the world – for this reason education of people is necessary. Due to serious congenital disorders associated with ZIKV infection and global impact of virus we suggest modifying old acronym TORCH for new TORZiCH to accent the position of Zika virus.</p>ARTICLE2019-10-18T00:00:00.000+00:00en-us-1