Heavy metals and their substances belong to widespread toxic polutions. They have great impact on vital functions of an organism. Heavy metals singly or by the simultaneous action of several elements, cause a series of chain reactions, causing metabolic disorders, toxic effects, leading to structural changes of abnormal behavior, or death of the body.
The aim of this review is to summarise the possible effect of zinck, lead, nickel, and cobalt on early embryo development.
Zinc, nickel, and cobalt, is essential for normal functioning of the organism. Nickel is part of the active center of the enzyme urease, hydrogenase. It is essential in small quantities for the metabolism of some taxonomic groups of plants. If nickel concentration increases this heavy metal has toxic effect. There are three basic mechanisms of toxicity of the metal for freshwater organisms, namely breach of ion exchange, respiration and growth inhibition of oxidative stress in cells. Zinc is the most abundant trace element. It is component of metallomes, which plays an important role in the metabolism of animals at all stages of their development, necessary for normal functioning of the body. Zinc in concentrations of 1.0 mg / L results in late hatching of zebrafish. It started on day 7 instead of the 4th, and in most cases without hatching embryos died at 11 and 12 days. In addition, developmental abnormalities observed such as abnormal embryogenesis, hatching low delay and loss of just hatching larvae and poor survival. Zinc in concentration of 1 × 10–4 M inhibits fertilization, causing deformities the embryo. Zinc deficiency has a negative impact on the development and reproduction, causing the development of abnormal eggs, changes in meiosis and ovulation processes, abnormal sperm and a high frequency of congenital anomalies. On the other hand higher amount of zinc ions are toxic. Zinc may play a role in various biological processes, such as enzyme activity, cell structures, protein structures, and carbohydrate metabolism in fish. Cobalt belongs to a group of vital micronutrients. Cobalt ion is a component of vitamin B12 and its deficiency directly affects the lack of vitamin B12. In physiological concentrations of cobalt is necessary for normal functioning of the body and an excess can cause various diseases. The effect of cobalt in the early stages of embryonic development and the mechanisms underlying its toxicity was conducted on zebrafish embryos fish.
Higher concentrations of cobalt results in abnormal development, including delayed hatching, abnormal morphology, retarded growth, and bradycardia. Oxidative stress and apoptosis caused by the toxic effect of cobalt in zebrafish embryos. Established dose-dependent effect on life expectancy cobalt embryos and larvae of zebrafish. It was that cobalt causes metabolic changes, such as reducing the rate of oxygen uptake and improve aerobic and anaerobic glycolysis, the single layer of dermal fibroblasts culture of rat embryo. Cobalt is extremely toxic in large doses. Lead has genotoxic and cytotoxic effect on fish embryo, affecting the integrity of chromosomes. Lead toxicity depends on the concentration and causes significant morphological abnormalities of the early stages of life. Genotoxic effects caused by lead acetate by chromosomal aberrations, and the increase in the number of micronuclei.
The analysis indicates that the zinc, nickel, lead, and cobalt at high doses may affect various metabolic processes in embryogenesis, leading to a slowdown in growth, morphological and functional abnormalities or death of the body.
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