Acrylamide (AA) is a highly reactive organic compound capable of polymerization to form polyacrylamide, which is commonly used throughout a variety of industries. Given its toxic effect on humans and animals, the last 20 years have seen an increased interest in research devoted to the AA. One of the main sources of AA is food. AA appears in heated food following the reaction between amino acids and reduced sugars. Large concentrations of AA can be found in popular staples such as coffee, bread or potato products. An average daily consumption of AA is between 0.3-2.0 µg/kg b.w. Inhalation of acrylamide is related with occupational exposure. AA delivered with food is metabolized in the liver by cytochrome P450. AA biotransformation and elimination result in formation of toxic glycidamide (GA). Both, AA and GA can be involved in the coupling reaction with the reduced glutathione (GSH) forming glutathione conjugates which are excreted with urine. Biotransformation of AA leads to the disturbance in the redox balance. Numerous research proved that AA and GA have significant influence on physiological functions including signal propagation in peripheral nerves, enzymatic and hormonal regulation, functions of muscles, reproduction etc. In addition AA and GA show neurotoxic, genotoxic and cancerogenic properties. In 1994, International Agency for Research on Cancer (IARC) classified acrylamide as a potentially carcinogenic substance to human.

The aim of this study was to investigate the effects of lead (Pb) and cadmium (Cd) content on basic motility characteristics (motility-MOT, progressive motility-PROG) as well as selected markers of the prooxidant-antioxidant balance (catalase-CAT, glutathione-GSH, malondialdehyde-MDA) in bovine seminal plasma and spermatozoa. Twenty five semen samples were collected from breeding bulls and used in the study. Motility analysis was carried out using the Computer Assisted Sperm Analysis (CASA) system. The samples were centrifuged, fractions of seminal plasma and spermatozoa were separated, lysates were prepared from the sperm cell fractions. Pb and Cd concentrations were determined by the voltametric method (ASV), antioxidants and MDA were analyzed by UV/Vis spectrophotometry. The analysis showed that the average concentration of Pb in the seminal plasma was 0.23 ± 0.02 μg/mL, while its amount in the sperm cells was significantly higher (0.41 ± 0.07 μg/mL; P < 0.05). The average Cd content in bovine seminal fractions was similar and non-significant: 0.09 ± 0.01 μg/mL in the seminal plasma and 0.11 ± 0.01 μg/mL in spermatozoa (P > 0.05). The correlation analysis revealed that both heavy metals were significantly negatively correlated with MOT and PROG (P < 0.05; P < 0.01; P < 0.001), CAT (P < 0.05; P < 0.01) as well as GSH (P < 0.05; P < 0.01) but significantly positively associated with MDA as the marker of lipid peroxidation (P < 0.05; P < 0.01). Moreover the samples were categorized in three quality groups (Excellent, Good, Moderate) according to their motility values. The lowest Pb, Cd and MDA concentrations but the best antioxidant characteristics were found in samples of the best quality, moderate quality samples exhibited the highest Pb, Cd and MDA content together with the worst antioxidant capacity. This study demonstrates that Pb and Cd are serious toxic elements, which are able to increase the risk of seminal oxidative stress development and a subsequent decrease of male fertility.

Exposure to xenobiotics causes pathophysiological changes in fish, including oxidative stress and neurotoxicity. Here, we describe the biochemical mechanisms underlying oxidative stress (i.e., redox imbalance) and the biochemical markers commonly used to assess its level. Neurotoxicity biomarkers used in fish include behavioral, histological, molecular, neurotransmitter-related, and enzymatic parameters, among which acetylcholinesterase (AChE) activity is the most commonly measured. We therefore also review the changes in AChE activity in fish exposed to common xenobiotics. In most cases, AChE activity decreased in a concentration- and time-dependent manner, although some studies reported no change or even an increase. We emphasize the relevance of all the parameters discussed in the context of fish toxicology studies.

The purpose of this study was to investigate the effect of alcohol exposure on liver and kidney antioxidant systems in taurine exhibition during different time periods. Mice were divided into groups: I – control; II – alcohol (2.5 g/kg b.w.); III – taurine (42.84 mg/kg b.w.); and IV – alcohol + taurine. Treatments were provided for 24 h, 14 days, and 56 days. In the liver and kidney of the alcohol group, antioxidant enzyme (superoxide dismutase, catalase, and glutathione peroxidase) activities, reduced glutathione (GSH), and malondialdehyde (MDA) levels were decreased, as compared to the control group in all time periods. Taurine was found to be effectively inhibiting oxidative action of alcohol and increasing all the tested parameters in the liver (after 24 h) and kidney (after 24 h and 14 days). Moreover, the positive effect of taurine administration on GSH and MDA levels persisted in the kidneys of mice exposed to alcohol for 56 days. In conclusion, alcohol administration led to a significant influence on antioxidant system in the liver and kidney, but simultaneous intake of taurine, along with ethanol, partly attenuated the antioxidant changes in these organs.

In this study, the human H295R adrenocarcinoma cell line was exposed to different concentrations (0.04, 0.2, 1.0, 2.5 or 5 µg/mL) of nonylphenol (NP) to investigate its impact on the inhibition or induction of the steroid hormones production during 48 h of in vitro culture. The hormone production was measured using ELISA kits. Results of this in vitro study suggest various effect of nonylphenol in relatively low concentrations on the selected steroid hormones production by the human H295R adrenocarcinoma cell line. The inhibiting impact on progesterone and androstenedione production was observed. The amount of progesterone was significantly decreased at 1.0, 2.5 and 5 µg/mL NP. Equally, the androstenedione production significantly decreased at 5 µg/mL NP. On the other hand, the amount of testosterone and 17β-estradiol was induced after nonylphenol exposition. The significant increase of testosterone level was found out at treatment with 5 µg/mL NP. 17β-estradiol production significantly increased at the doses of 2.5 and 5 µg/mL NP.

Alcohol is one of the most commonly consumed neurotoxins by humans. Its negative effect on bone health is known for a long time. However, its impact on qualitative and quantitative 2D characteristics of the compact bone is still unclear. Therefore, the aim of this study was to investigate in detail the effects of subchronic alcohol exposure on compact and trabecular bone tissues microstructure of laboratory mice using 2D and 3D imaging methods. Ten clinically healthy 12 weeks-old mice (males) were randomly divided into two groups. Animals from experimental group (group E; n = 5) drank a solution composed of 15% ethanol and water (1.7 g 100% ethanol kg−1 b.w. per day) for 8 weeks, while those from control group (group C; n = 5) drank only water. Subchronic exposure to alcohol leads to several changes in qualitative 2D characteristics of the compact bone such as the presence of primary vascular radial bone tissue in pars anterior of endosteal border and a higher number of resorption lacunae (five times more) in the middle part of substantia compacta. Morphometrical 2D evaluations of the compact bone showed significantly increased sizes of primary osteons’ vascular canals (p < 0.05) in mice from the experimental group (E group). Sizes of Haversian canals and secondary osteons were not affected by alcohol consumption. In mice from the E group, significantly lower values for relative bone volume and bone mineral density of the compact bone were observed. In the trabecular bone, decreased values for bone volume, trabecular number, trabecular thickness and bone surface (p < 0.05) were documented. Alcohol decreased not only bone volume and density of the compact bone, but it also reduced trabecular bone volume and leads to trabecular thinning. It caused vasodilation of primary osteons’ vascular canals and increased porosity in the compact bone.