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Thymol is a natural essential oil derived from the plant Thymus vulgaris L. It is known to be beneficial for human and animal health and has been used in beekeeping practice against Varroa mite for years. In this study, the genotoxic and antigenotoxic potential of thymol were evaluated on the honey bee (Apis mellifera L.) continuous cell line AmE-711 for the first time. Using the Comet assay, three increasing concentrations (10, 100, and 1000 µg/mL) of thymol were tested. Negative control (non-treated cells) and positive control (cells treated with 100 µM H2O2) were also included. The absence of thymol cytotoxicity was confirmed with the Trypan blue exclusion test. Thymol in the concentration of 10 µg/mL did not increase DNA damage in AmE-711 honey bee cells, while 100 and 1000 µg/mL concentrations showed genotoxic effects. For testing the antigenotoxic effect, all concentrations of thymol were mixed and incubated with H2O2. The antigenotoxic effect against was absent at all concentrations (10, 100, 1000 μg/mL) tested. Moreover, thymol enhanced the H2O2-induced DNA migration in the Comet assay. The obtained results indicate genotoxic effects of thymol on cultured honey bee cells suggesting its careful application in beekeeping practice to avoid possible negative effects on honey bees.

Diabetes, a chronic group of medical disorders characterized byhyperglycemia, has become a global pandemic. Some hormones may influence the course and outcome of diabetes, especially if they potentiate the formation of reactive oxygen species (ROS). There is a close relationship between thyroid disorders and diabetes. The main objective of this investigation was to find out whether peripheral blood mononuclear cells (PBMCs) are more prone to DNA damage by triiodothyronine (T3) (0.1, 1 and 10 μM) at various stages of progression through diabetes (obese, prediabetics, and type 2 diabetes mellitus—T2DM persons). In addition, some biochemical parameters of oxidative stress (catalase-CAT, thiobarbituric acid reactive substances—TBARS) and lactate dehydrogenase (LDH) were evaluated. PBMCs from prediabetic and diabetic patients exhibited increased sensitivity for T3 regarding elevated level of DNA damage, inhibition of catalase, and increase of TBARS and LDH. PBMCs from obese patients reacted in the same manner, except for DNA damage. The results of this study should contribute to a better understanding of the role of thyroid hormones in the progression of T2DM.

Thyroid hormones stimulate aerobic metabolism which may lead to oxidative stress accompanied by damage to various cellular macromolecules, including DNA. Previous comet assay studies have shown that thyroid hormones cause DNA damage due to the creation of reactive oxygen species (ROS). However, cytogenetic studies have been equivocal because although an increase in the sister-chromatid exchange frequency per cell has been reported increased micronuclei frequency has not. We used cytogenetic examination of chromosome breakage and aberrations in whole-blood cultures of human peripheral blood lymphocytes to investigate possible clastogenic effects when lymphocytes were exposed to 0.002 µM to 50 µM of L-thyroxine for 24 h and 48 h, these concentrations being chosen because they had been used in previous studies of sister-chromatid exchange and micronuclei frequency. Under our experimental conditions thyroxine did not induced any statistically significant increase in chromosome breakage or aberrations. This lack of clastogenic effects is in contrast to the reported comet assay results obtained using purified lymphocytes, possibly because whole-blood cultures contain catalase and glutathione peroxidase capable of reducing the effects of reactive oxygen species.

There is a widely accepted view that the endogenous substances, includinghormones, do not have any mutagenous effect when present in the usualphysiological concentrations. However, beside relative stability and permanence ofthe genetic material, its changeability is also needed to provide for the biologicalevolution. Thus, it is possible to expect that certain reactions, due to the complexity ofthe mechanism of the signal transduction under the effect of hormones, still! lead tothe creation of reactive derivatives able to inter-react with the DNA molecules thusencouraging the emergence of mutations. This paper gives a survey of the explorationof the hormones' genotoxic effects in various test-systems, namely, from the bactericthrough the ćeli cultures and experiments in vivo upon laboratory guinea-pigs, up tothe determination of the mutagenous effects in the people that were treated byhormones. The steroid hormones' effects are described in detail in the literaturewhile, on the other hand, there is not sufficient knowledge yet about possible changesof the genetic material under the influence of the non-steroid hormones. Theexaminations of the steroid hormones' geonotoxicity in the bacterial systems havemainly given negative results. Tn more complex eukaryotic systems in vitro and invivo most of the steroid hormones manifest mutagenous effects, though the resultmay vary depending one the type of ćeli or the biological species used in theexperiment. As for the non-steroid hormones, though they have been studied less, itseems that they do not mostly express mutagenous effects. Today it is clear that thesteroid hormones (especially estrogen) are completely carcinogenic and that they arecapable of encouraging the process of carcinogenesis both by inducing covalentsimulating the cell division (tumor promoters).