Obesogens in Foods.

Obesogens, as environmental endocrine-disrupting chemicals, are supposed to have had an impact on the prevalence of rising obesity around the world over the last forty years. These chemicals are probably able to contribute not only to the development of obesity and metabolic disturbances in individuals, but also in their progeny, having the capability to epigenetically reprogram genetically inherited set-up points for body weight and body composition control during critical periods of development, such as fetal, early life, and puberty. In individuals, they may act on myriads of neuro-endocrine-immune metabolic regulatory pathways, leading to pathophysiological consequences in adipogenesis, lipogenesis, lipolysis, immunity, the influencing of central appetite and energy expenditure regulations, changes in gut microbiota-intestine functioning, and many other processes. Evidence-based medical data have recently brought much more convincing data about associations of particular chemicals and the probability of the raised risk of developing obesity. Foods are the main source of obesogens. Some obesogens occur naturally in food, but most are environmental chemicals, entering food as a foreign substance, whether in the form of contaminants or additives, and they are used in a large amount in highly processed food. This review article contributes to a better overview of obesogens, their occurrence in foods, and their impact on the human organism.

Long-Term Monitoring of the Antibody Response to a SARS-CoV-2 Infection.

A group of 110 patients from the West Bohemian region who had been infected with COVID-19 was monitored for the purposes of this study. We focused on cases of mild or moderate COVID-19; statistically the most likely to occur. Day zero was defined as the day on which a positive PCR test was first established. The mean length of observation was 6.5 months, the maximum length 12 months. The first blood samples were taken from a smaller cohort during the 1-3 months following the first positive PCR test. We assumed that SARS-CoV-2 antibodies would be present during this period and therefore a limited number of samples were taken for the purpose of detecting antibodies. More samples were collected, starting 4 months after the first positive PCR test. A subsequent set of blood samples were drawn, mostly 6 months after the first ones. Our study confirmed the presence of total IgG SARS-CoV-2 antibodies up to 1 year after the onset of the disease. The peak of antibody production was observed in the third month after the first positive PCR test. A mathematical estimate of the median duration of antibody positivity was calculated to be 18 months from the onset of the COVID-19 infection.

The Role of Serum Tumor Markers in Follow-up After Surgical Treatment of Malignant Lung Tumors.

AIM: The aim of this study was to evaluate the utility of selected tumor markers for the detection of lung cancer recurrence during follow-up. PATIENTS AND METHODS: The study group consisted of 109 patients and 109 healthy controls. The following biomarkers were selected: Carcinoembryonic antigen; cytokeratin fragment 19; neuron-specific enolase; tissue polypeptide-specific antigen; cytokeratin fragments 8, 18 and 19; insulin-like growth factor 1; pro-gastrin-releasing peptide; and 25-hydroxyvitamin D. The biomarkers were assessed individually or using a multivariate analysis. RESULTS: Carcinoembryonic antigen [area under the receiver operating characteristics curve (AUC)=0.6857, p<0.0001] and cytokeratin fragment 19 (AUC=0.6882, p<0.0001) proved best in detecting relapse. The multivariate model indicated insulin-like growth factor 1 (p=0.0006, AUC=0.6225) as the third most useful biomarker. The multivariate model using these three markers achieved the best AUC value of 0.7730 (p=0.0050). CONCLUSION: We demonstrated that carcinoembryonic antigen and cytokeratin fragment 19 play a key role in the detection of lung cancer recurrence. A multivariate approach can increase the effectiveness of detection.

Chronic DDE Exposure Modifies Mitochondrial Respiration during Differentiation of Human Adipose-Derived Mesenchymal Stem Cells into Mature Adipocytes.

The contribution of environmental pollutants to the obesity pandemic is still not yet fully recognized. Elucidating possible cellular and molecular mechanisms of their effects is of high importance. Our study aimed to evaluate the effect of chronic, 21-day-long, 2,2-bis (4-chlorophenyl)-1,1-dichlorethylenedichlorodiphenyldichloroethylene (p,p'-DDE) exposure of human adipose-derived mesenchymal stem cells committed to adipogenesis on mitochondrial oxygen consumption on days 4, 10, and 21. In addition, the mitochondrial membrane potential (MMP), the quality of the mitochondrial network, and lipid accumulation in maturing cells were evaluated. Compared to control differentiating adipocytes, exposure to p,p'-DDE at 1 µM concentration significantly increased basal (routine) mitochondrial respiration, ATP-linked oxygen consumption and MMP of intact cells on day 21 of adipogenesis. In contrast, higher pollutant concentration seemed to slow down the gradual increase in ATP-linked oxygen consumption typical for normal adipogenesis. Organochlorine p,p'-DDE did not alter citrate synthase activity. In conclusion, in vitro 1 µM p,p'-DDE corresponding to human exposure is able to increase the mitochondrial respiration per individual mitochondrion at the end of adipocyte maturation. Our data reveal that long-lasting exposure to p,p'-DDE could interfere with the metabolic programming of mature adipocytes.

Expression of classical mediators in hearts of rats with hepatic dysfunction.

Liver cirrhosis is associated with impairment of cardiovascular function including alterations of the heart innervation, humoral and nervous dysregulation, changes in systemic circulation and electrophysiological abnormalities. Choline acetyltransferase (ChAT), enzyme forming acetylcholine, tyrosine hydroxylase (TH), and dopamine-ß-hydroxylase (DBH), enzymes participating in noradrenaline synthesis, are responsible for the production of classical neurotransmitters, and atrial natriuretic peptide (ANP) is produced by cardiomyocytes. The aim of this study was to evaluate the influence of experimentally induced hepatic dysfunction on the expression of proANP, ChAT, TH, and DBH in the heart. Hepatic dysfunction was induced by application of thioacetamide (TAA) or by ligation of bile duct. Biochemical parameters of hepatic injury and levels of peroxidation in the liver and heart were measured. Liver enzymes measured in the plasma were significantly elevated. Cardiac level of peroxidation was increased in operated but not TAA group animals. In the left atrium of operated rats, the expression of TH and DBH was lower, while expression of ChAT remained unchanged. In TAA group, no significant differences in the expression of the genes compared to controls were observed. Liver injury induced by ligation leads to an imbalance in the intracardiac innervation, which might impair nervous control of the heart.

Effect of chromium (VI) exposure on antioxidant defense status and trace element homeostasis in acute experiment in rat.

Occupational exposure to hexavalent chromium (Cr(VI)) compounds is of concern in many Cr-related industries and their surrounding environment. Cr(VI) is a proven toxin and carcinogen. The Cr(VI) compounds are easily absorbed, can diffuse across cell membranes, and have strong oxidative potential. Despite intensive studies of Cr(VI) pro-oxidative effects, limited data exist on the influence of Cr(VI) on selenoenzymes thioredoxin reductase (TrxR) and glutathione peroxidase (GPx)-important components of antioxidant defense system. This study investigates the effect of Cr(VI) exposure on antioxidant defense status, with focus on these selenoenzymes, and on trace element homeostasis in an acute experiment in rat. Male Wistar rats (130-140g) were assigned to two groups of 8 animals: I. control; and II. Cr(VI) treated. The animals in Cr(VI) group were administered a single dose of K2Cr2O7 (20 mg /kg, intraperitoneally (ip)). The control group received saline solution. After 24 h, the animals were sacrificed and the liver and kidneys were examined for lipid peroxidation (LP; thiobarbituric acid reactive substances (TBARS) concentration), the level of reduced glutathione (GSH) and the activities of GPx-1, TrxR-1, and glutathione reductase (GR). Samples of tissues were also used to estimate Cr accumulation and alterations in zinc, copper, and iron levels. The acute Cr(VI) exposure caused an increase in both hepatic and renal LP (by 70%, p < 0.01 and by 15%, p < 0.05, respectively), increased hepatic GSH level and GPx-1 activity, and decreased renal GPx-1 activity. The activity of GR was not changed. A significant inhibitory effect of Cr(VI) was found on TrxR-1 activity in both the liver and the kidneys. The ability of Cr(VI) to cause TrxR inhibition could contribute to its cytotoxic effects. Further investigation of oxidative responses in different in vivo models may enable the development of strategies to protect against Cr(VI) oxidative damage.

Differential influences of various arsenic compounds on antioxidant defense system in liver and kidney of rats.

In this study, oxidative stress-related parameters and As retention were examined in liver and kidneys of male Wistar rats exposed to arsenic trioxide, sodium arsenite (iAsIII), sodium arsenate (iAsV), and dimethylarsinic acid (DMAsV) at a single ip dose of 3.8 mgAs/kgbw, at 24h post-exposure. In liver, lipid peroxidation increased in iAsIII-exposed rats, glutathione peroxidase activity decreased in inorganic arsenic (iAs)-exposed rats, and catalase and thioredoxin reductase activities decreased significantly in all As-exposed groups. Both As(III) and As(V) exposure elevated GSH level with no effect on glutathione reductase activity. In kidneys, catalase activity decreased significantly in iAs-exposed, rats; GSH level, glutathione reductase and thioredoxin reductase activity decreased in DMAsV-treated, rats. The tissue As retention was higher in kidneys compared to liver and was also higher in As(III)-exposed compared to As(V)-exposed rats. The results demonstrate similar potency of inorganic As(III) and As(V) compounds to inhibit/induce antioxidant defense system, with liver being more vulnerable to acute As(III)- and As(V)-induced oxidative stress.

The influence of curcumin and manganese complex of curcumin on cadmium-induced oxidative damage and trace elements status in tissues of mice.

Curcumin (diferuoyl methane) from turmeric is a well-known biologically active compound. It has been shown to ameliorate oxidative stress and it is considered to be a potent cancer chemopreventive agent. In our previous study the antioxidative effects of curcumin in cadmium exposed animals were demonstrated. Also manganese exerts protective effects in experimental cadmium intoxication. The present study examined the ability of the manganese complex of curcumin (Mn-curcumin) and curcumin to protect against oxidative damage and changes in trace element status in cadmium-intoxicated male mice. Curcumin or Mn-curcumin were administered at equimolar doses (0.14 mmol/kg b.w.) for 3 days, by gastric gavages, dispersed in methylcellulose. One hour after the last dose of antioxidants, cadmium chloride (33 micromol/kg) was administered subcutaneously. Both curcumin and Mn-curcumin prevented the increase of hepatic lipid peroxidation -- expressed as MDA level, induced by cadmium intoxication and attenuated the Cd-induced decrease of hepatic GSH level. No change in hepatic glutathione peroxidase or catalase activities was found in Cd-exposed mice. A decreased GSH-Px activity was measured in curcumin and Mn-curcumin alone treated mice. Neither curcumin nor Mn-curcumin treatment influenced cadmium distribution in the tissues and did not correct the changes in the balance of essential elements caused by Cd-treatment. The treatment with Mn-curcumin increased the Fe and Mn content in the kidneys of both control and Cd-treated mice and Fe and Cu content in the brain of control mice. In conclusion, regarding the antioxidative action, introducing manganese into the curcumin molecule does not potentiate the studied effects of curcumin.

The effect of curcumin on cadmium-induced oxidative damage and trace elements level in the liver of rats and mice.

The present study was designed to investigate in acute animal experiments the effects of oral curcumin pre-treatment (50 mg/kg body weight per day for 3 days) on liver oxidative damage and trace element changes caused by cadmium chloride administration (0.025 mmol/kg to rats and 0.03 mmol/kg to mice, s.c., 1h after the last curcumin treatment). In rats, the level of Cd-induced lipid peroxidation (320% of controls) was significantly lowered by curcumin pre-treatment (165% of controls), and was accompanied by significant increase of glutathione (GSH) level in both Cd-treated and Cd plus curcumin-treated group. In mice, the Cd-induced lipid peroxidation (125% of controls) was abolished by curcumin treatment. Concurrently, a depletion of GSH was found in the liver of both Cd-treated (67% of controls) and Cd plus curcumin-treated mice (54% of controls). Curcumin treatment did not change cadmium (Cd) distribution and did not cause systematic alterations in trace element status.