To assess hepatotoxicity and to determine the underlying mechanisms of carbamazepine (CBZ) toxicity in fish, histopathology and the liver proteome were examined after Chinese rare minnow (Gobiocypris rarus) were exposed to 1, 10, and 100 μg/L CBZ for 28 days. Histopathological changes included disruption of spatial structure, pyknotic nuclei, cellular vacuolization and deformation of cell nuclei, in addition to marked swelling of hepatocytes in all treatment groups. Protein analysis revealed that there were gender-specific responses in rare minnow following exposure, and there were 47 proteins in females and 22 proteins in males identified as differentially abundant following CBZ treatments. Pathway analysis revealed that cellular processes affected by CBZ included apoptosis, cell differentiation, cell proliferation, and the respiratory chain, indicating impaired energy homeostasis. Noteworthy was that 15 proteins identified as different in abundance were associated with carcinogenicity. Relative mRNA levels for select transcripts were consistent with the changes of proteins N-myc downstream regulated gene (NDRG), Tropomyosin 2-Beta (TPM2) and annexin A4 (ANXA4). Protein pyruvate kinase, liver and RBC (PKLR) were increased at 1 and 100 μg/L CBZ without significant difference in transcript levels. These findings characterize molecular responses and histological changes in the liver that generate new insights into CBZ hepatotoxicity in Chinese rare minnow.

Using scanning electron microscopy (SEM) and transmission electron microscopy (TEM) analysis, it was found that the ultrastructure of chloroplasts were changed, the shape of the chloroplasts altered and the numbers of grana that were asymmetrical increased; the numbers of grana and thylakoids decreased under the stress of Cd and Zn. The results indicated that the complex pollution involving Cd and Zn resulted in the membrane system of chloroplasts being damaged. When external phosphorus was applied, the numbers of damaged chloroplasts were significantly reduced and the nucleoli were better formed than those that did not receive phosphorus treatment. Moreover, many phosphate deposits were found in the vacuoles and on the surface of the roots, which were formed by phosphorus complexing with Cd (Ksp = 2.53 x 10-33) and Zn (Ksp = 9.00 x 10-33), respectively. Treatment with phosphorus conduced an increased chlorophyll content in plants compared with those that did not receive external phosphorus. External P could decrease the bioavailability of Cd and Zn.

Organisms are increasingly exposed to ultraviolet (UV) rays of sunlight, due to the thinning of the ozone layer and its widespread use in sterilization processes, especially against the SARS-CoV-2 virus. The present study was conducted with the purpose of evaluating the damages of UV-A and UV-C radiations in Allium cepa L. roots. The effects of two different types of UV on some physiological, biochemical, cytogenotoxic, and anatomical parameters were investigated in a multifaceted study. Three groups were formed from Allium bulbs, one of which was the control group. One of the other groups was exposed to 254 nm (UV-C) and the other to 365 nm (UV-A) UV. Growth retardation effect of UV was investigated with respect to germination percentage, total weight gain, and root elongation, while cytogenotoxicity arisen from UV exposure was analyzed using mitotic index (MI) and chromosomal aberration (CA) and micronucleus (MN) frequency. Oxidative stress due to UV application was investigated based on the accumulation of malondialdehyde (MDA) and the total activities of superoxide dismutase (SOD) and catalase (CAT) enzymes. Also, anatomical changes induced by UV-A and UV-C were analyzed in root meristematic cells. UV treatments caused significant reductions in growth-related parameters. Both UV treatments caused a significant increase in MDA levels and induction of SOD and CAT enzymes in root meristematic cells. A decrease in MI and an increase in the frequency of MN and CAs were observed in root tip cells, indicating the cytogenotoxic effect of UV application. Anatomical damages such as epidermis cell damage, cortex cell damage, necrotic zones, giant cell nucleus, and indistinct transmission tissue occurred in cells exposed to UV. All of the physiological, biochemical, cytogenetic, and anatomical damages observed in this study were more severe in cells treated with UV-C compared to UV-A. This study suggested that UV exposure triggered growth inhibition, cytogenotoxicity, oxidative stress, and meristematic cell damages in A. cepa roots depending on the wavelength.

The aim of the present work was to determine peculiarities of accumulation of ionic state 137Cs in model experiments with seedlings of spring wheat (Triticum aestivum L., “Nandu”) using laboratory experiments and to evaluate the complex effect of 137Cs ionizing radiation and geochemical factors on the growth of this plant. 137Cs accumulation in seedlings is influenced by the presence of mineral substances in the nutritional medium and by the conditions of illumination. Mineral substances (K+, Ca2+, Mg2+, Cu2+, NH4 +, P5+, Fe3+) reduced the 137Cs accumulation coefficient of seedlings approximately three times. Addition of heavy metals as well as anionic group NO3 − to the growth medium caused insignificant changes in the level of radionuclide accumulation. In the model systems of RNA synthesis with wheat seedling cells nuclei isolated after complex treatment (in vivo) by 137Cs and HM showed clear inhibition of the RNA-polymerase II. This inhibition manifested itself as a complex effect of 137Cs ionizing radiation and heavy metals.

Fish are bioindicators of water pollution, and an increased rate of their erythrocyte nuclear morphological abnormalities (ENMAs)—and particularly of erythrocyte micronuclei (EMN)—is used as a genotoxicity biomarker. Despite the potential value of ENMAs and MN, there is scarce information about fish captured in Iberian estuaries. This is the case of the Portuguese estuaries of the Mondego, Douro and Ave, suffering from different levels of environmental stress and where chemical surveys have been disclosing significant amounts of certain pollutants. So, the aim of this study was to evaluate genotoxicants impacts and infer about the exposure at those ecosystems, using the grey mullet (Mugil cephalus) as bioindicator and considering the type and frequency of nuclear abnormalities of erythrocytes as proxies of genotoxicity. Sampling of mullets was done throughout the year in the important Mondego, Douro and Ave River estuaries (centre and north-western Portugal). The fish (total n = 242) were caught in campaigns made in spring–summer and autumn–winter, using nets or fishing rods. The sampled mullets were comparable between locations in terms of the basic biometric parameters. Blood smears were stained with Diff-Quik to assess the frequencies of six types of ENMAs and MN (given per 1,000 erythrocytes). Some basic water physicochemical parameters were recorded to search for fluctuations matching the ENMAs. Overall, the most frequent nucleus abnormality was the polymorphic type, sequentially followed by the blebbed/lobed/notched, segmented, kidney shaped, vacuolated, MN and binucleated. The total average frequency of the ENMAs ranged from 73 ‰ in the Mondego to 108 ‰ in the Ave. The polymorphic type was typically ≥50 % of the total ENMAs, averaging about 51 ‰, when considering all three estuaries. The most serious lesion—the MN—in fish from Mondego and Douro had a similar frequency (≈0.38 ‰), which was significantly lower than that in the Ave (0.75 ‰). No significant seasonal differences existed as to the MN rates and seasonal differences existed almost only in the Douro, with the higher values in AW. In general, the pattern of ENMAs frequencies was unrelated with the water physicochemical parameters. Considering the data for both the total ENMAs and for each specific abnormality, and bearing in mind that values of MN in fish erythrocytes >0.3 ‰ usually reflect pollution by genotoxicants, it is suggested that mullets were likely being chronically exposed to such compounds, even in the allegedly less polluted ecosystem (Mondego). Moreover, data supported the following pollution exposure gradient: Mondego < Douro < Ave. The scenario and inferences nicely agree with the published data from chemical monitoring.

The cytogenetic toxicity of rhodamine B on root tip cells of Allium cepa was investigated. A. cepa were cultured in water (negative control), 10 ppm methyl methanesulfonate (positive control), and three concentrations of rhodamine B (200, 100, and 50 ppm) for 7 days. Rhodamine B inhibited mitotic activity; increased nuclear anomalies, including micronuclei, nuclear buds, and bridged nuclei; and induced oxidative stress in A. cepa root tissues. Furthermore, a substantial amount of long nucleoplasmic bridges were entangled together, and some nuclei were simultaneously linked to several other nuclei and to nuclear buds with nucleoplasmic bridges in rhodamine B-treated cells. In conclusion, rhodamine B induced cytogenetic effects in A. cepa root tip cells, which suggests that the A. cepa root is an ideal model system for detecting cellular interactions.

The aim of the present study was to comparatively evaluate genomic damage (micronucleus) and cellular death (pyknosis, karyolysis, and karyorrhexis) in exfoliated oral mucosa cells from crack cocaine users by micronucleus test. A total of 30 crack cocaine users and 30 health controls (non-exposed individuals) were included in this setting. Individuals had epithelial cells from cheek mechanically exfoliated, placed in fixative, and dropped in clean slides, which were checked for the above nuclear phenotypes. The results pointed out significant statistical differences (p < 0.05) of micronucleated oral mucosa cells from crack cocaine users. Exposure to crack cocaine caused an increase of other nuclear alterations closely related to cytotoxicity such as karyolysis in oral cells as well. In summary, these data indicate that crack cocaine is able to induce chromosomal breakage and cellular death in oral mucosa cells of users.

Insecticides and their residues are known to cause several types of ailments in human body. An attempt had been made to assess digitally the geno-toxicity of methyl parathion (MP) and chlorpyrifos (CP) to in vitro-grown HepG2 cell line, with Hoechst 33342 staining, comet, and micronucleus assays. Additionally, “acridine orange/ethidium bromide” (AO/EB) staining was done for the determination of insecticide-induced cytotoxicity, in corollary. Hoechst 33342 staining of cells revealed a decrease in live cell counts at 8–40 mg/L MP and 15–70 mg/L CP. Moreover, nuclear fragmentations in ranges 8 to 40 mg/L MP and 15 to 70 mg/L CP were recorded dependant on individual doses, increasingly with concomitant increases in comet tail length values. DNA fragmentation index measured in comet assays was 94.3 ± 0.57 at 40 mg/L MP and 93.3 ± 2.08 at 70 mg/L CP. Average micronuclei number was 59.0 ± 2.00 at 40 mg/L MP and 62.6 ± 1.52 at 70 mg/L CP, per 1000 cell nuclei, in micronucleus assay. Minimum inhibitory concentration (MIC) values with AO/EB staining for monitoring cytotoxicity were 4 and 10 mg/L for MP and CP, respectively. Lethal concentration₅₀ (LC₅₀) values were 20.89 mg/L MP and 79.43 mg/L CP in AO/EB staining, for cytotoxicity with probit analyses. It was concluded that MP was comparatively more geno-toxic than CP to HepG2 cell. It was discernible that at lower levels of each insecticide, geno-toxicity was recorded in comparison to cytotoxicity.