Metals in wine can originate from both natural and anthropogenic sources, and its concentration can be a significant parameter affecting consumption and conservation of wine. Since metallic ions have ...important role in oxide–reductive reactions resulting in wine browning, turbidity, cloudiness, and astringency, wine quality depends greatly on its metal composition. Moreover, metals in wine may affect human health. Consumption of wine may contribute to the daily dietary intake of essential metals (i.e., copper, iron, and zinc) but can also have potentially toxic effects if metal concentrations are not kept under allowable limits. Therefore, a strict analytical control of metal concentration is required during the whole process of wine production. This article presents a critical review of the existing literature regarding the measured metal concentration in wine, methods applied for their determination, and possible sources, as well as their impact on wine quality and human health. The main focus is set on aluminum, arsenic, cadmium, chromium, copper, iron, manganese, nickel, lead, and zinc, as these elements most often affect wine quality and human health.
Toxic metals are extensively found in the environment, households, and workplaces and contaminate food and drinking water. The crosstalk between environmental exposure to toxic metals and human ...diseases has been frequently described. The toxic mechanism of action was classically viewed as the ability to dysregulate the redox status, production of inflammatory mediators and alteration of mitochondrial function. Recently, growing evidence showed that heavy metals might exert their toxicity through microRNAs (miRNA)-short, single-stranded, noncoding molecules that function as positive/negative regulators of gene expression. Aberrant alteration of the endogenous miRNA has been directly implicated in various pathophysiological conditions and signaling pathways, consequently leading to different types of cancer and human diseases. Additionally, the gene-regulatory capacity of miRNAs is particularly valuable in the brain-a complex organ with neurons demonstrating a significant ability to adapt following environmental stimuli. Accordingly, dysregulated miRNAs identified in patients suffering from neurological diseases might serve as biomarkers for the earlier diagnosis and monitoring of disease progression. This review will greatly emphasize the effect of the toxic metals on human miRNA activities and how this contributes to progression of diseases such as cancer and neurodegenerative disorders (NDDs).
Indoor dust presents an important source of daily exposure to toxic elements. The present study reports for the first time the levels of Al, As, Cd, Co, Cr, Cu, Fe, Mn, Mo, Ni, Pb, Sb, Sn, Se, Sr, ...Tl, V, and Zn measured in dust samples collected from 10 kindergartens and 21 cars from Zagreb, Croatia. Based on the obtained data, we assessed the health risks from overall daily exposure to trace elements for children aged 2–6 years taking into account three pathways of dust intake—ingestion, dermal absorption, and inhalation. The median concentration of most elements was significantly higher in dust obtained from cars compared to kindergartens, especially in the cases of Co (11.62 vs. 3.60 mg kg−1), Cr (73.55 vs. 39.89 mg kg−1), Cu (186.33 vs. 26.01 mg kg−1), Mo (8.599 vs. 0.559 mg kg−1), Ni (37.05 vs. 17.38 mg kg−1), and Sn (9.238 vs. 1.159 mg kg−1). Oral intake was identified as the most important exposure pathway, except for Cr, Ni, and Sb where dermal contact was the main route of exposure. Health risk assessment indicated that no adverse effects are expected from overall exposure to trace elements. Although the cases of high exposure to toxic elements are not common in areas with no significant environmental pollutants, due to the health threat they may present even at low levels, their status should be carefully monitored.
Official control of EU market foodstuffs repeatedly reports high nicotine levels in dried wild mushrooms without any clear scientific consensus about their origin. The advised constant monitoring ...calls for improvements to existing methods. For this purpose, our aim was to develop a headspace solid phase microextraction (HS-SPME) method coupled to gas chromatography with mass spectrometric detection (GC-MS) that would eliminate the need for extensive sample pre-treatment. The type of fiber coating, amount of sample, extraction temperature and time, desorption time and salt addition were investigated and optimized as parameters affecting the SPME procedure. The optimized conditions were used to validate a quantitative method for nicotine analysis by matrix-matched calibration and isotopically labelled internal standard correction. The method provided good linearity (
r
2
= 0.9994) over the tested concentration range (0.0251 mg kg
1
), low detection limit (0.005 mg kg
1
) and low quantification limit (0.017 mg kg
1
) for nicotine, being below the EU foodstuff regulations. For both of the tested concentration levels (0.050 and 0.200 mg kg
1
), precision expressed as relative standard deviation was below 10% (4.5% and 8.5%, respectively), while accuracy was 98.2% and 100.3%. The optimized method was then used to determine nicotine levels in 18 samples of dried
Boletus
mushrooms from southeastern European countries entering the EU market. We demonstrated our HS-SPME procedure to be fast, simple, sensitive, solvent-free, cost-effective and thus suitable for controlling consumer safety regarding nicotine level in dried mushrooms.
New HS-SPME-GC-MS method is characterized by high sensitivity and efficiency using a single stage organic solvent-free extraction and low sample mass.
Nanotechnology has the potential to provide formulations of antitumor agents with increased selectivity towards cancer tissue thereby decreasing systemic toxicity. This
in vivo
study evaluated the ...potential of novel nanoformulation based on poly(lactic-
co
-glycolic acid) (PLGA) to reduce the cardiotoxic potential of doxorubicin (DOX).
In vivo
toxicity of PLGADOX was compared with clinically approved non-PEGylated, liposomal nanoformulation of DOX (LipoDOX) and conventional DOX form (ConvDOX). The study was performed using Wistar Han rats of both sexes that were treated intravenously for 28 days with 5 doses of tested substances at intervals of 5 days. Histopathological analyses of heart tissues showed the presence of myofiber necrosis, degeneration processes, myocytolysis, and hemorrhage after treatment with ConvDOX, whereas only myofiber degeneration and hemorrhage were present after the treatment with nanoformulations. All DOX formulations caused an increase in the troponin T with the greatest increase caused by convDOX. qPCR analyses revealed an increase in the expression of inflammatory markers IL-6 and IL-8 after ConvDOX and an increase in IL-8 expression after lipoDOX treatments. The mass spectra imaging (MSI) of heart tissue indicates numerous metabolic and lipidomic changes caused by ConvDOX, while less severe cardiac damages were found after treatment with nanoformulations. In the case of LipoDOX, autophagy and apoptosis were still detectable, whereas PLGADOX induced only detectable mitochondrial toxicity. Cardiotoxic effects were frequently sex-related with the greater risk of cardiotoxicity observed mostly in male rats.
Nanoformulations decrease systemic toxicity effects of antitumor agents.
The present study reports for the first time the levels of 7 polybrominated diphenyl ether (PBDE) congeners and 11 polycyclic aromatic hydrocarbons (PAH) measured in dust samples collected in 10 ...kindergartens, 11 workplaces, and 25 cars from Zagreb, Croatia. ΣPBDEs mass fractions were 3.11–14.42, <LOD‐313.75, and 0.6–5666.98 ng g−1 dust, while ΣPAHs were 244.9–833.0, 230.5–5632.7, and 395.6–12114.8 ng g−1 dust in kindergartens, workplaces, and cars, respectively. In the central case scenario, dust from homes contributed to the intake of PBDEs and PAHs the most, while for PBDEs in the worst‐case scenario, the intake through car dust prevailed. Carcinogenic and non‐carcinogenic risks were assessed for PAHs and PBDEs, respectively, for two age groups (adults and toddlers) and for professional drivers as a specific group. The hazard index for adults, toddlers, and professional drivers for PBDEs was less than 1 indicating that there is no significant risk of non‐carcinogenic effects due to exposure to these chemicals. Total carcinogenic risk for PAHs was negligible for all groups in the central case scenario, but the Incremental Lifetime Cancer Risk values >10−6 in the worst‐case scenario indicated a potential risk, especially for professional drivers. Also, in the cases of elevated contaminant levels, toddlers are susceptible to a higher risk, despite the short time they spend in cars.
Terbuthylazine belongs to the chloro-s-triazine group of herbicides and acts primarily as a photosynthesis inhibitor. The mechanisms of action related to its exposure, relevant both in animals and ...humans, are still insufficiently investigated. This comprehensive study focused on the outcomes of terbuthylazine exposure at cell level in vitro, and a mice model in vivo. Experiments in vitro were conducted on whole human peripheral blood, isolated lymphocytes, and HepG2 cells exposed for 4 h to terbuthylazine at 8.00, 0.80, and 0.58 ng/mL, which is comparable with current reference values set by the European Commission in 2011. Terbuthylazine cytotoxicity was evaluated using dual fluorescent staining with ethidium bromide and acridine orange on lymphocytes, and CCK-8 colorimetric assay on HepG2 cells. The levels of DNA damage were measured using alkaline and hOGG1-modified comet assays. The potency of terbuthlyazine regarding induction of oxidative stress in vitro was studied using a battery of standard oxidative stress biomarkers. The in vivo experiment was conducted on Swiss albino mice exposed to terbuthlyazine in the form of an active substance and its formulated commercial product Radazin TZ-50 at a daily dose of 0.0035 mg/kg bw for 14 days. Following exposure, the DNA damage levels in leukocytes, bone marrow, liver, and kidney cells of the treated mice were measured using an alkaline comet assay. In vitro results suggested low terbuthylazine cytotoxicity in non-target cells. The highest tested concentration (8.00 ng/mL) reduced lymphocyte viability by 15%, mostly due to apoptosis, while cytotoxic effects in HepG2 cells at the same concentration were negligible. Acute in vitro exposure of human lymphocytes and HepG2 cells to terbuthylazine resulted in low-level DNA instability, as detected by the alkaline comet assay. Further characterization of the mechanisms behind the DNA damage obtained using the hOGG1-modified comet assay indicated that oxidative DNA damage did not prevail in the overall damage. This was further confirmed by the measured levels of oxidative stress markers, which were mostly comparable to control. Results obtained in mice indicate that both the active substance and formulated commercial product of terbuthylazine produced DNA instability in all of the studied cell types. We found that DNA in liver and kidney cells was more prone to direct toxic effects of the parent compound and its metabolites than DNA in leukocytes and bone marrow cells. The overall findings suggest the formation of reactive terbuthylazine metabolites capable of inducing DNA cross-links, which hinder DNA migration. These effects were most pronounced in liver cells in vivo and HepG2 cells in vitro. To provide a more accurate explanation of the observed effects, additional research is needed. Nevertheless, the present study provides evidence that terbuthylazine at concentrations comparable with current reference values possesses toxicological risk because it caused low-level DNA instability, both at cellular and animal organism level, which should be further established in forthcoming studies.
The decline of male fertility has become a serious public health concern over the last decades, coinciding with an increase in environmental exposure to toxic pollutants. Toxic elements cadmium (Cd), ...arsenic (As), and lead (Pb) seem to contribute to declining fertility in men through progressive impairment of semen quality. Reproductive toxicity of these elements is mediated by multiple mechanisms. Although experimental animal studies generally support an adverse role of Cd, As, and Pb in human reproduction issues, data on the effects induced by the levels of toxic elements that represent environmental exposure are inconsistent. This review summarizes reports from experimental studies in animals and epidemiological observational findings from environmental exposure to Cd, As, and Pb, with special focus on semen quality parameters as the indicator of male fertility.
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•Cd, As, and Pb are important reproductive toxicants.•Toxicity mechanisms include oxidative stress, apoptosis, inflammation, and endocrine disruption.•Low-level exposure to Cd, As, and/or Pb may impair semen quality parameters in men.•Additional epidemiological studies including general population are recommended.
Imidacloprid is a neonicotinoid insecticide that acts selectively as an agonist on insect nicotinic acetylcholine receptors. It is used for crop protection worldwide, as well as for non-agricultural ...uses. Imidacloprid systemic accumulation in food is an important source of imidacloprid exposure. Due to the undisputable need for investigations of imidacloprid toxicity in non-target species, we evaluated the effects of a 28-day oral exposure to low doses of imidacloprid (0.06 mg/kg b. w./day, 0.8 mg/kg b. w./day and 2.25 mg/kg b. w./day) on cholinesterase activity, oxidative stress responses and primary DNA damage in the blood and brain tissue of male Wistar rats. Exposure to imidacloprid did not cause significant changes in total cholinesterase, acetylcholinesterase and butyrylcholinesterase activities in plasma and brain tissue. Reactive oxygen species levels and lipid peroxidation increased significantly in the plasma of rats treated with the lowest dose of imidacloprid. Activities of glutathione-peroxidase in plasma and brain and superoxide dismutase in erythrocytes increased significantly at the highest applied dose. High performance liquid chromatography with UV diode array detector revealed the presence of imidacloprid in the plasma of all the treated animals and in the brain of the animals treated with the two higher doses. The alkaline comet assay results showed significant peripheral blood leukocyte damage at the lowest dose of imidacloprid and dose-dependent brain cell DNA damage. Oral 28-day exposure to low doses of imidacloprid in rats resulted in detectable levels of imidacloprid in plasma and brain tissue that directly induced DNA damage, particularly in brain tissue, with slight changes in plasma oxidative stress parameters.
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•Male Wistar rats were orally exposed to low doses of imidacloprid for 28 days.•Detectable levels of imidacloprid were found in plasma and brain tissue.•Imidacloprid induced slight changes in oxidative stress parameters.•Primary DNA damage was dose-dependent in brain cells.
Although considered a good alternative to organophosphate pesticides, there are reports indicating adverse effects of neonicotinoid insecticides on reproduction. Our aim was to assess the effects of ...exposure to low doses of imidacloprid on antioxidant state, DNA damage, and concentration of essential elements in the testes and epididymis using a rat model. Adult male Wistar rats were orally treated with doses comparable to currently proposed health-based reference values: 0.06 (ADI), 0.80 (10× AOEL), or 2.25 (1/200 LD
) mg/kg b.w./day for 28 consecutive days. Exposure to 2.25 mg/kg b.w./day of imidacloprid resulted in a significantly lower testis weight (1.30 ± 0.17 g compared to 1.63 ± 0.15 g in controls). Treatment with 0.06 mg/kg b.w./day increased the level of reduced glutathione in the epididymis (73%), while the activities of epididymal glutathione peroxidase and superoxide dismutase significantly increased in all treated rats (74-92% and 26-39%, respectively). Exposure to imidacloprid resulted in a low, but significant, level of DNA damage in testicular sperm cells regardless of the concentration applied (<28% compared to the negative control). Higher concentrations of Mo were measured in the testes of rats treated with 0.80 and 2.25 mg/kg b.w./day (72.9 ± 7.9 and 73.9 ± 9.1 mg/g, respectively) compared to the control animals (60.5 ± 7.8 mg/g). Higher concentrations of Na were measured in the testes of rats treated with 2.25 mg/kg b.w./day (1679 ± 82 mg/g compared to 1562 ± 56 mg/g in controls). The fact that such low doses of imidacloprid were able to produce measurable biological effects calls for the further evaluation of this widely used insecticide.
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