Synthesis of Poly-N,N–Dialylaminoethanoic Acid and Investigation of his Mutagenic Action on the Test System Drosofila Melanogaster

The resulting monomer is N,N-diallylaminoethanoic acid and a polymer based on it. The structure of the monomer and polymer is confirmed by physicochemical methods. The toxic properties of poly-N,N-diallylaminoethanoic acid were investigated on the Drosophila melanogaster test system. The results obtained allow us to conclude that poly-N,N-diallylaminoethanoic acid in concentrations of 1 % does not have a toxic effect.

The Effect of Pesticides on the Tomato Bacterial Speck Disease Pathogen Pseudomonas Syringae pv. Tomato

A significant part of the used pesticides does not reach the target organisms and, while remaining in the agrophytocenosis, influences all living organisms in it. Having a toxic and often mutagenic effect, pesticides induce morphological and physiological changes in the cells of microorganisms and are the cause of phenotypic heterogeneity of their populations. However, the effect of pesticides on phytopathogenic bacteria as non-target microorganisms remains out of the field of view for most researchers. However, the use of pesticides can lead to expansion of the diversity of existing phytopathogens and, as a consequence, complications of identification of the pathogens, loss of resistance by plants varieties, and increased harm from diseases caused by them. This study is focused on the effect of pesticides used in tomato plantations on the causative agent of bacterial speck of this crop—Pseudomonas syringae pv. tomato. The studies were carried out using the methods of classical microbiology. The mutagenic action of pesticides was recorded, taking into account the increase of the number of streptomycin resistance mutations in bacteria in the case of pesticide action. It is established that the fungicide aluminium phosethyl is characterised by a bacteriostatic effect on P. syringae pv. tomato. Deltamethrin insecticide does not affect the growth of P. syringae pv. tomato. However, there is an increase in the frequency of streptomycin resistance mutations in both studied strains of P. syringae pv. tomato after using deltamethrin. It is shown that the frequency of occurrence of R (rough colonies) forms of P. syringae pv. tomato IZ28 and IZ46 after using deltamethrin increased by 100 times when in comparison to the frequency of spontaneous morphological dissociation, or smooth-to-rough (S-R) mutation, of these bacteria. Therefore, aluminium phosethyl is characterised by moderate bacteriostatic action against P. syringae pv. tomato. Deltamethrin does not influence the growth of the pathogen of tomato speck but increases the frequency of formation of StrR mutants and R forms of phytopathogenic bacteria.

Anti-mutagenic Action of Ruta chalepensis against Rat Sperm Cell Abnormalities-induced by Potassium Bromate

Aims: The aim of current study was to investigate the genotoxic damage of potassium bromate on sperm cell morphology and the potential defense role of Ruta chalepensis (Rue) against the potassium bromate effects. Study Design: Fifty rats (Strain: Rattus norvegicus) were randomly divided into five groups (10 rats/group) as follows: (Control group) received distilled water daily for 4 weeks, (KBrO3 group) treated with KBrO3 (100 mg/kg/b.w) for 4 weeks, (Rue group) received Rue orally in a daily dose (0.5 g/animal) for 4 weeks, (treatment group) were first provided with oral doses of KBrO3 daily for 2 weeks and then treated orally with KBrO3 in association with Rue for an additional 2 weeks Finally (protective group) was administered with Rue orally for 2 weeks and then administered oral doses of Rue in association with KBrO3 for an additional 2 weeks. Place and Duration of Study: Department of Zoology and Department of Botany, University of Omar Almukhtar, between July 2018 and September 2019. Methodology: Sperm suspensions, filtered and smears were made according to the standard protocol for sperm morphology assay. The smears were fixed, allow to dry and stained with hematoxylin and then washed under slow running water until the excess stain is removed and were putted in eosin dye. Results: The results were showed that potassium bromate has the ability to cause mutations in the morphology of sperm cells. The highest mutation rates of head, tail and neck reached 16.60, 5.200 and 3.200 respectively in animals. Several types of sperm abnormalities such as hock free, banana type, amorphous, hummer shape after the administration of potassium bromate comparing with the negative control animals that treated only with potassium bromate. On the other hand, the oil extract of Ruta chalepensis significantly inhibited the mutations by declining the abnormality rates of head, tail and neck to 2.600, 1.600 and 0.400 in protective group. Thus, potassium bromate has to be considered as a conceivable line regarding human health. Conclusion: Potassium bromate clearly caused a wide range of sperm cell abnormalities and Rue oil extracts have a good anti-mutagenic effects against potassium bromate by decreasing the sperm cell abnormalities.

Cadmium and its inorganic compounds - expressed as Cd - inhalable fraction. Documentation of proposed values of occupational exposure limits (OELs)

Cadmium (Cd) is a white metal with a bluish tint. It forms a number of compounds occurring in them on the degree of oxidation 2+. Cadmium compounds are water-soluble to varying degrees. The highest risk groups include employees involved in the production of nickel-cadmium batteries, alloys, cadmium pigments as well as employees of non-ferrous metal smelters and cutting welders of metals covered with a cadmium anti-corrosion layer. According to the Central Register of Data on Exposure to Substances , Preparations, Factors or Technological Processes on Carcinogenic or Mutagenic Action, 4276 workers in Poland were exposed to cadmium and its compounds. Cadmium is absorbed into the body through inhalation and digestive systems. In humans, the absorption is 2–50% and 4–6%, respectively. Elimination of cadmium from the body is a slow process. The estimated half-life of cadmium is from 5 to 30 years. Results of studies conducted in subjects exposed to cadmium in the work environment showed that the threshold concentration of cadmium in urine, at which increased excretion of low molecular weight proteins in urine was found, is 5–10 µg/g creatinine. In 1993, IARC identified cadmium and its compounds as a human carcinogen (group 1). The results of experimental studies in rats provided evidence of cadmium carcinogenicity as a result of inhalation exposure. Cadmium is recognized by SCOEL as a category C carcinogen, i.e. as a genotoxic carcinogen for which a threshold of action (concentration) can be determined, also called a practical threshold. The critical organs for the toxic effects of cadmium and its inorganic compounds in humans, depending on the route of exposure, are kidneys, lungs and possibly bones. The critical effect of cadmium on kidneys is increased excretion of low molecular weight proteins in urine, while the critical effect on lungs is the carcinogenic effect. Inhalation studies in rats exposed to cadmium at concentrations of 30 µgCd/m3, 13.4 µgCd/m3 and 10 µgCd/m3 for 18 months were used as the basis to propose TLV-TWA. The concentration of 10 µg Cd/m3 was taken as the NOAEL value. After applying the formula and taking into account the uncertainty factors with a total value of 10, the concentration of 0.001 mg/m3 (1 µgCd/m3) was determined as the TLV-TWA value for the inhaled fraction. Biological monitoring is the best indicator of cadmium exposure. The excretion of cadmium in urine enables the assessment of cumulative cadmium in the body and takes into account all sources of cadmium exposure, including contaminated food and smoking, while the blood cadmium concentration is a measure of current exposure. Previous BEI values in blood and urine were 5 μgCd/l and 5 μgCd/g creatinine, respectively. After discussion at the 91st meeting of the Interministerial Committee for TLVs and PELs, these values were maintained as mandatory. This article discusses the problems of occupational safety and health, which are covered by health sciences and environmental engineering.

The mutagen and carcinogen cadmium is a high-affinity inhibitor of the zinc-dependent MutLα endonuclease

MutLα (MLH1-PMS2 heterodimer), which acts as a strand-directed endonuclease during the initiation of eukaryotic mismatch repair, has been postulated to function as a zinc-dependent enzyme [Kosinski J, Plotz G, Guarné A, Bujnicki JM, Friedhoff P (2008) J Mol Biol 382:610–627]. We show that human MutLα copurifies with two bound zinc ions, at least one of which resides within the endonuclease active site, and that bound zinc is required for endonuclease function. Mutagenic action of the carcinogen cadmium, a known inhibitor of zinc-dependent enzymes, is largely due to selective inhibition of mismatch repair [Jin YH, et al. (2003) Nat Genet 34:326–329]. We show that cadmium is a potent inhibitor (apparent Ki ∼ 200 nM) of MutLα endonuclease and that cadmium inhibition is reversed by zinc. We also show that inhibition of mismatch repair in cadmium-treated nuclear extract is significantly reversed by exogenous MutLα but not by MutSα (MSH2-MSH6 heterodimer) and that MutLα reversal depends on integrity of the endonuclease active site. Exogenous MutLα also partially rescues the mismatch repair defect in nuclear extract prepared from cells exposed to cadmium. These findings indicate that targeted inhibition of MutLα endonuclease contributes to cadmium inhibition of mismatch repair. This effect may play a role in the mechanism of cadmium carcinogenesis.

3,3'-Dimethylbenzidine and its salts – inhalable fraction. Documentation of proposed values of occupational exposure limits (OELs)

3,3'-Dimethylbenzidine (3,3'-DMB, DMB, o-tolidine) is a solid used (as water-soluble dihydrochloride salt (dimethylbenzidine · 2HCl)) in the production of azopigments, polyurethane elastomers and plastics for coating. Small amounts are also used in diagnostic tests in laboratories. Occupational exposure to dimethylbenzydine occurs mainly during the production and use of pigments to dye textiles, plastics, paper and leather. In 2005–2014, dimethylbenzidine was used in Poland in 18–30 workplaces, where 135–280 people each year (mainly women) were exposed. No epidemiological data and information related to toxic effects of DMB in humans was found in the available literature. The LD50 value (median lethal dose) after single intragastric administration of 3,3'-dimethylbenzidine to rats was 404 mg/kg. After repeated exposure of laboratory animals, liver, kidney, thyroid injury and hematological changes were noted. In the Ames tests with metabolic activation, it was found that metabolites of 3,3'-dimethylbenzidine show stronger mutagenic action than the parent compound. 3,3'-DMB induced also chromosome aberrations and exchange of sister chromatids in in vitro tests. Although 3,3'-dimethylbenzidine is a derivative of carcinogenic benzidine, carcinogenic effects on humans have not been proven. However, research provides data about carcinogenic effect of 3,3'-DMB in animals. After subcutaneous administration of 3,3'-dimethylbenzidine and its dihydrochloride salt in drinking water, Zymbal's and mammary glands tumors, and cancers of uterus, skin, liver, hematopoietic system, small and large intestine were observed in rats. IARC classified 3,3'-dimethylbenzidine in the 2B group (a supposed carcinogenic agent for humans), whereas ACGIH – in the A3 group (proved carcinogenic effect on animals and unknown carcinogenic effect for humans). The European Union (according to the CLP classification) has listed 3,3'-DMB in the 1B category with the inscription "H350 – can cause cancer". The permissible concentrations for 3,3'-dimethylbenzidine have been established in some European countries only (Austria, Slovenia and Switzerland) as 0.03 mg/m3. The basis of the proposed maximum concentration value (MAC-TWA) for 3,3'-dimethylbenzidine and its salts was a risk assessment of cancer in male rats chronically exposed to 3,3'-dimethylbenzidine dihydrochloride in drinking water. Taking into account the cancer risk at the level of 10-4, a concentration of 0.03 mg/m3 for the MAC-TWA value was proposed. There are no basis to determine the short-term value (STEL) and biological limit values (BLV). It was also proposed to label the compound with "Carc 1B", which indicates that it is a carcinogen category 1B, and "skin" – the absorption of substances through the skin may be as important as an inhalation route.

Effect of aqueous extract of Rosemary officinalis on cytotoxicity of CCL4 induced albino male mice

This study focused the line on the effect of aqueous extract of Rosemary officinalis, as well as, effect of toxic compound CCL4, on micronucleus formation and mitotic index assay in albino male mice. This work started at September 2017 at Biotechnology Research center \Al-Nahrain University, by using 20 albino male mice. The result indicated that aqueous extract of rosemary caused significant increased in mitotic index and decrease micronucleus formation for two doses tested 50,100 mg/kg in comparison with negative and positive controls, also the results revealed that CCL4 showed significant mutagenic action on biological system of treated mice by increased frequency of micronucleus formation and decreased the percentage of mitotic index in bone marrow cells. Pre-and post –treatment between aqueous extract and CCL4 were also made. The results of pre and post treatment with rosemary extract were also caused a significant decreased in micronucleus formation and increase the percentage of mitotic index for two doses 50,100 mg/kg in comparison with its corresponding controls which caused increased in the frequencies of micronucleus formation and decrease the percentage of mitotic index in bone marrow cells. Conclusions: Rosemary officinalis enhanced immunity, reduced mutagenic effects against cytotoxicity of CCL4.