The mussel-watch concept was firstly proposed in 1975, which was later adopted by several international monitoring programs worldwide. However, for the very first time, a field experiment with caged mussels was performed in three reservoirs in Bulgaria to follow the harmful effects of sub-chronic pollution (30 days) of metals, trace, and macro-elements, as well as some organic toxicants, such as polybrominated diphenyl ethers and chlorinated paraffins. Therefore, we studied the biometric indices, histochemical lesions in the gills, biochemical changes in the digestive glands (antioxidant defense enzymes, such as catalase, glutathione reductase, and glutathione peroxidase; metabolic enzymes, such as lactate dehydrogenase, alanine aminotransferase, and aspartate aminotransferase, and the neurotransmitter cholinesterase), in addition to the DNA damage in the Chinese pond mussel, Sinanodonta woodiana (Lea, 1834) in Kardzhali, Studen Kladenets and Zhrebchevo reservoirs in Bulgaria. Significant correlation trends between the pollution levels, which we reported before, and the biomarker responses were established in the current paper. Overall, we found that both tested organs were susceptible to pollution-induced oxidative stress. The different alterations in the selected biomarkers in the caged mussels compared to the reference group were linked to the different kinds and levels of water pollution in the reservoirs, and also to the simultaneously conducted bioaccumulation studies.

Cyclin-dependent kinases (CDKs) are crucial regulators of the eukaryotic cell cycle. The critical role of CDK2 in the progression of meiosis was demonstrated in a single mammalian species, the mouse. We used immunocytochemistry to study the localization of CDK2 during meiosis in seven rodent species that possess hetero- and homomorphic male sex chromosomes. To compare the distribution of CDK2 in XY and XX male sex chromosomes, we performed multi-round immunostaining of a number of marker proteins in meiotic chromosomes of the rat and subterranean mole voles. Antibodies to the following proteins were used: RAD51, a member of the double-stranded DNA break repair machinery; MLH1, a component of the DNA mismatch repair system; and SUN1, which is involved in the connection between the meiotic telomeres and nuclear envelope, alongside the synaptic protein SYCP3 and kinetochore marker CREST. Using an enhanced protocol, we were able to assess the distribution of as many as four separate proteins in the same meiotic cell. We showed that during prophase I, CDK2 localizes to telomeric and interstitial regions of autosomes in all species investigated (rat, vole, hamster, subterranean mole voles, and mole rats). In sex bivalents following synaptic specificity, the CDK2 signals were distributed in three different modes. In the XY bivalent in the rat and mole rat, we detected numerous CDK2 signals in asynaptic regions and a single CDK2 focus on synaptic segments, similar to the mouse sex chromosomes. In the mole voles, which have unique XX sex chromosomes in males, CDK2 signals were nevertheless distributed similarly to the rat XY sex chromosomes. In the vole, sex chromosomes did not synapse, but demonstrated CDK2 signals of varying intensity, similar to the rat X and Y chromosomes. In female mole voles, the XX bivalent had CDK2 pattern similar to autosomes of all species. In the hamster, CDK2 signals were revealed in telomeric regions in the short synaptic segment of the sex bivalent. We found that CDK2 signals colocalize with SUN1 and MLH1 signals in meiotic chromosomes in rats and mole voles, similar to the mouse. The difference in CDK2 manifestation at the prophase I sex chromosomes can be considered an example of the rapid chromosome evolution in mammals.

For the first time, this study investigates in vivo the potential of Na-modified natural clinoptilolite to mitigate cadmium toxicity in ICR mice, a model relevant to human health. We enhanced natural clinoptilolite to improve its cadmium (Cd) exchange capacity. Mice were exposed to environmentally realistic cadmium nitrate Cd(NO₃)₂ doses in their drinking water. The detoxification efficacy of the mineral was evaluated over 45 days in four groups: control (no supplementation), Cd(NO₃)₂ only, clinoptilolite only, and a combination of Cd(NO₃)₂ and clinoptilolite. We assessed Cd bioaccumulation in the liver and kidneys, genotoxicity (micronucleus assay), hematological parameters, and oxidative stress markers. Cd exposure resulted in significant bioaccumulation, reduced growth, changes in erythrograms, DNA damage, and oxidative stress. Mice receiving clinoptilolite alone showed a significant increase in body mass. Modified clinoptilolite led to a nearly 48% reduction in Cd accumulation and a 30% increase in Cd excretion in the Cd-plus-clinoptilolite group compared to the Cd-only group. Erythrogram and leukogram parameters returned to near-normal levels, with reductions in malondialdehyde (MDA) and increases in glutathione (GSH) observed by the end of the experiment. No elevated levels of micronuclei were found following clinoptilolite supplementation. These results suggest that modified clinoptilolite may be a cost-effective detoxifier in Cd-polluted regions.