Resveratrol ameliorates ortho- polychlorinated biphenyls' induced toxicity in ovary cells.

Polychlorinated biphenyls (PCBs) can induce chronic oxidative stress, inflammation, and cell death, leading to coronary heart disease, endothelial dysfunction, neurotoxicity, cancer, obesity, type 2 diabetes, reproductive dysfunction, etc. The aim of this study was to investigate possible protective effect of resveratrol (2.5-20 µM) in ovarian cells exposed to PCBs. An emphasis was on identifying mechanisms of resveratrol action upon distinct structure of the individual PCB congener-planar dioxin-like PCB 77 and non-planar di-ortho-substituted PCB 153. Multiple toxicity endpoint analysis was performed. Cell viability/proliferation was assessed by Trypan Blue exclusion method, Neutral Red, Kenacid Blue, and MTT bioassays. The level of oxidative stress was measured by fluorescent probes, and flow cytometry was applied to evaluate the mode of cell death. Resveratrol applied alone did not affect cell proliferation and viability in doses up to 20 µM, although significant antioxidative activity was observed. Toxic effects of ortho-PCB 153 (cytotoxicity, oxidative stress, and cell death) were mitigated by resveratrol. On the contrary pre-incubation with resveratrol did not result in cell viability protection when planar PCB 77 was applied. This indicates that resveratrol efficacy may be linked to specific structure of the individual congener, suggesting nutritional modulation of environmental insults caused by ortho-PCBs. We point out the importance of resveratrol dosage considering that synergistic cytotoxic effect with both PCB congeners is observed at concentrations ≥ 10 µM.

Compositional Changes in the Extra Virgin Olive Oil Used as a Medium for Cheese Preservation.

The influence of semi-hard (C1), hard (C2), and soft whey cheese (C3) immersed in extra virgin olive oil (EVOO) on its oxidative and hydrolytic parameters, fatty acids, and phenolic composition during two months of simultaneous storage was investigated. Accelerated hydrolytic and oxidative degradation was noted in EVOO stored with the immersed cheese compared to control oil. Oxidation indicator (K232), myristic (C 14:0), and trans-oleic fatty acid (C18:1t) exceeded the prescribed limit for the EVOO category in oils stored with immersed C1 and C2, which indicated that standard analytical parameters are ineffective as tools to examine the declared quality and authenticity of such topping oils. The noted changes in fatty acid profile were primarily prescribed to the migration of fats. C1 and C2 influenced a comparable reduction in EVOO total identified phenolic content (-92.1% and -93.5%, respectively), despite having a different content of total proteins and moisture, whereas C3 influenced a slightly lower reduction (-85.0%). Besides the protein profile, other cheese compounds (e.g., moisture, carbohydrates) have been shown to have a considerable role in the development of the EVOO phenolic profile. Finally, compositional changes in EVOO used as a medium for cheese preservation are under significant influence of the cheese's chemical composition.

Cell membrane-related toxic responses and disruption of intercellular communication in PCB mechanisms of toxicity: A review.

An understanding of polychlorinated biphenyl (PCB) congener-specific effects on cell membrane and intercellular communication is important within the studies of PCB absorption, organ-related PCB accumulation and exertion of toxic responses. Toxic potential of PCBs is linked to various deleterious effects on human health, including neurotoxicity, immunotoxicity, reproductive toxicity and genotoxicity and, recently in 2016 International Agency for Research on Cancer (IARC) has upgraded the classification of PCBs to Group 1 "Carcinogenic to humans." Proposed mechanisms of aforementioned PCBs adverse effects at cellular membrane level are: (i) downregulation of gap junction intercellular communication and/or connexins; (ii) compromised membrane integrity; and (iii) altered tight junction barrier function. This study, based on an extensive literature survey, shows the progress in scientific research of each of these three levels with the aim of pointing out the earliest toxic events of PCBs, which can result in serious cell/tissue/organ damage.

Mycotoxins in food and feed.

Mycotoxins represent secondary fungal metabolites not essential to the normal growth and reproduction of a fungus, but capable of causing biochemical, physiological and pathological changes in many species. Harmful effects of mycotoxins observed in humans and animals include carcinogenicity, teratogenicity, immune toxicity, neurotoxicity, hepatotoxicity, nephrotoxicity, reproductive and developmental toxicity, indigestion and so forth. These substances can be found in a variety of very important agricultural and food products, primarily dependent of product moisture content, and its water activity, relative air humidity, temperature, pH value, composition of the food matrix, the degree of its physical damage, and the presence of mold spores. Given that industrial processing has no significant effect on their reduction and in order to be able to vouch for the absence of mycotoxins, it is necessary to process foodstuffs under standardized and well-controlled conditions and to control each and every loop of the food production and storage chain. Preventative measures capable of reducing the contamination to the minimum must be in place and should be exercised by all means. In case that contamination does happen, methods for mycotoxin reduction or elimination should be implemented in dependence on a number of parameters such as properties of food or feed. Further research is needed in order to identify conditions that facilitate the growth of mycotoxin-producing fungi and develop effective preventative measures that can reduce contamination of food and feed as also to recognize possible synergistic effects of different mycotoxins in organism.

Cytotoxicity of gamma irradiated aflatoxin B1 and ochratoxin A.

Toxicity of gamma irradiated mycotoxins aflatoxin B1 (AFB1) and ochratoxin A (OTA) was investigated in vitro. AFB1 and OTA stock solutions (50 mM, in methanol) were gamma irradiated (5 and 10 kGy) and non-irradiated and irradiated mycotoxins solutions were tested for cytotoxicity on Pk15, HepG2 and SH-SY5Y cell lines (MTT assay, 1-500 µM concentration range; 24 h exposure). Degradation of mycotoxin molecules was examined by liquid chromatography tandem mass spectrometry (HPLC-MS/MS). AFB1 and OTA radiolytic products were less toxic than the parent mycotoxins to all of the tested cell lines. Gamma irradiation even at 5 kGy had effect on AFB1 and OTA molecules however, this effect was dependent on chemical structure of mycotoxin. Since gamma irradiation at low dose reduced initial level of both mycotoxins, and gamma irradiated mycotoxins had lower toxicity in comparison to non-irradiated mycotoxins, it can be concluded that gamma irradiation could be used as decontamination method.

Mutagenicity and DNA-damaging potential of clenbuterol and its metabolite 4-amino-3,5-dichlorobenzoic acid in vitro.

The aim of this study was to evaluate in vitro toxicity of clenbuterol and its metabolite 4-amino-3,5-dichlorobenzoic acid. Cytotoxicity and pro-oxidative effect of both compounds were studied on human colon adenocarcinoma cell line SW 480. No significant cytotoxic effect of either compound was observed. Results of an Ames test on Salmonella typhimurium did not indicate mutagenic activity of clenbuterol on TA 98 and TA 100 strains, regardless of metabolic activation. Potential mutagenic effects of the highest clenbuterol concentration (2500 ng/ml) were observed on the TA 1535 strain. The obtained results of alkaline comet assay on isolated human lymphocytes suggested that both compounds induced an increase of primary DNA damage in a concentration-dependent manner. 4-ADBA was a slightly more potent inducer of primary DNA damage as compared to clenbuterol. Chromosomal aberration analysis showed that clenbuterol caused a statistically significant increase in the total number of aberrant cells only at the highest concentration tested (3% vs. 0.7% in the negative control). The results of this study might represent a solid frame for designing and planning future studies with both compounds, which should further clarify their mechanisms of action and genotoxic/cytogenetic effects relevant for human risk assessment.

Biochemical changes in pig serum after ochratoxin A exposure.

The objective of this study was to investigate the effect of ochratoxin A (OTA) on serum biochemical parameters of pigs during subchronic treatment with 300 µg OTA/kg of feed for 30 days. OTA treatment resulted in significantly higher (p < 0.05) serum levels of creatinine, urea, potassium and alkaline phosphatase, and significantly lower levels of glucose and total protein. These changes in serum biochemical parameters in treated pigs were indicative of impaired liver and kidney function caused by OTA exposure.

Serum luteinizing hormone response to administration of gonadotropin-releasing hormone to atrazine-treated gilts.

The aim of the study was to evaluate the response of porcine luteinizing hormone (pLH) in serum to a single iv administration of gonadotropin-releasing hormone (GnRH) in atrazine-treated pigs. Experiments were performed in 15 mature female pigs (10 atrazine-treated, 5 control). From the onset of estrous (day 0), the pigs were given 1 mg atrazine/kg body mass in feed for 20 d of the estrous cycle. On the last day, blood samples were collected at min 0 from control and atrazine-exposed, and 5 atrazine-exposed pigs were immediatey given 100 mg GnRH iv. Blood samples were collected from atrazine-exposed and the GnRH-injected atrazine-exposed groups at 20, 30, 40 and 90 min and serum pLH concentrations were determined by radioimmunoassay. The administration of atrazine led to significant (p< 0.001) suppression of serum pLH concentrations (0.57 +/- 0.05 ng/ml) compared to control animals (2.24 +/- 0.20 ng/ml). The single iv GnRH administration to the atrazine-exposed pigs provoked significant pLH release at 20 and 30 min after GnRH administration, indicating attenuation of GnRH release in the atrazine-exposed animals was responsible for the suppression of serum pLH.