Ecology/6. Environmental monitoring.

PhD Daribai, A.O., Masalimov, Zh.K.

Eurasian National University named after L.N. Gumilev

The effects of heavy metals on the catalase activity level in blood serum

Oxidative stress represents an imbalance between the production and manifestation of reactive oxygen species (ROS) and a biological system's ability to readily detoxify the reactive intermediates or to repair the resulting damage. (ROS) such as hydrogen peroxide, superoxide and hydroxyl radical are products of oxygen metabolism in all aerobic organisms products of the action of ionizing radiation, heavy metals, chemical mutagens and carcinogens. Hydroxyl radicals and singlet oxygen are very reactive towards DNA in comparison with superoxide and hydrogen peroxide action. However, in the presence of ions of heavy metals, both superoxide and hydrogen peroxide are converted to the highly reactive hydroxyl radical in vitro. ROS are among the most important environmental genotoxic factors [1]. ROS are known to directly attack vital cellular components, including proteins, lipids, and nucleic acids and oxidative damage to biomolecules (oxidative stress). When ROS attack DNA, oxidized bases are frequently generated [2]. ROS cause predominantly base damage in DNA, forming more than 20 base lesions have been identified (thymine glycols, 5-hydroxycytosine, 8-oxo-7,8-dihydro-2′-deoxyguanosine (8-oxodG, 8-oxoguanine), 8-oxoadenine (8-hydroxyadenine), the formamidopyrimidine derivatives of purines, etc.), only a fraction of these have received appreciable study, most notably 8-oxodG. It occurs most readily at guanine residues due to the high oxidation potential of this base relative to cytosine, thymine, and adenine. 8-oxodG exhibits ambiguous encoding properties in the biosynthesis of nucleic acids, behaving as guanine and thymine during replication [3] and as guanine and uracil during transcription [4], because it can pair with cytosine and mispair with adenine in the syn conformation. The miscoding properties of 8-oxodG have been implicated in such biological processes as mutagenesis [1,5,6], producing predominantly G→T transversions replication [3,4,7], carcinogenesis [7,8], aging [9], and some age-dependent diseases [10,11]. This type of DNA damage is repaired by specific enzymes which excise 8-oxodG from DNA. Increased level of 8-oxodG in DNA is a biological marker of physiological distress of the body, because it is involved in many diseases: atherosclerosis, Parkinson's disease, heart failure, myocardial infarction, Alzheimer's disease, schizophrenia, bipolar disorder, fragile X syndrome [12], and chronic fatigue syndrome, but short-term oxidative stress may also be important in prevention of aging by induction of a process named mitohormesis.

Heavy metal pollution of environment is widespread across the globe and has caused biological problems, leading to potential toxicity to living organisms. For example recent research found that the atmospheric input of heavy metals to agricultural systems also significantly contributed to metal loading in soil. These complicated pathways of contamination make it difficult to avoid the exposure to the metals existing in our surroundings.

Heavy metal pollution of soil is widespread across the globe and has caused biological problems, leading to potential toxicity to living organisms. Recent research found that the atmospheric input of heavy metals to agricultural systems also significantly contributed to metal loading in soil. These complicated pathways of contamination make it difficult to avoid the exposure to the metals existing in our surroundings. This paper focuses on the study of formation of 8-oxodG in mammalian DNA in comparison with level of lipid peroxidation under heavy metal action, in vivo.

Metal-induced toxicity and carcinogenicity, with an emphasis on the generation and role of reactive oxygen and nitrogen species is reviewed. ROS are known to directly attack vital cellular components, including proteins, lipids, and nucleic acids and oxidative damage to biomolecules. Metal-mediated formation of free radicals causes various modifications to DNA bases, enhanced lipid peroxidation, and altered calcium and sulfhydryl homeostasis.

We used 2-month male mice (SHK) maintained on a standard diet ad libitum, weighing 20 grams in the experiments. Mice were subjected to single exposure of 15.7mM CuSO₄, 25.1mM CuCl, 25mM CrO₃, 16.4 mM FeSO₄, 15.5mM ZnSO₄, 7.5mM Pb(NO₃)₂ per each animal. Introduction of heavy metal aqueous solution was carried out through intraperitoneal injections.

We studied the effect of these metals on the level of catalase activity in blood serum Table 1.

Table 1. Catalase activity (mol N₂O₂/ml/min) in blood serum under the influence of heavy metal ions

Name	МDА, мМ
Control	0,6±0,051
15.7mM CuSO4	0,32±0,06
25.1mM CuCl	0,48±0,02
25mM CrO3	0,36±0,08
16.4 mM FeSO4	0,29±0,08
15.5mM ZnSO4	0,58±0,03
7.5mM Pb(NO3)2	0,41±0,06

The analysis of catalase activity in blood serum under the influence of heavy metal ions showed its declining Table 1. The most negative impact on catalase activity showed the ions of divalent copper, chromium and iron.

The level of catalase activity under the influence of these metals decreased in approximately 2 times compared with the control and was 0.29 to 0.36 mole Н₂О₂/ml/min.

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