Lead does not succumb to biological decomposition, and its ability to accumulate in the body makes it a serious threat to the health of people and animals, while affecting the reproductive function. In most cases, poisoning with lead remains asymptomatic. In a number of studies the authors concluded that in men the level of lead in the blood more than >40 μg/dL leads to the disorder of reproductive functions, such as low libido, a small sperm volume, the amount of spermatozoa, an increase in the abnormal morphology of spermatozoa and decrease in their motility. Male factors are considered the main cause of infertility in 40% of infertile couples and contribute to the emergence of this state in combination with female factors in 20% of cases. The mechanisms of how lead causes male infertility are covered in depth. It is assumed that the basic effect on the reproductive function of men is likely to occur due to changes in the reproductive hormonal axis and hormonal control of spermatogenesis, and not due to direct toxic effects on the seminiferous tubules. The adverse effect of lead on the male reproductive function, especially at low doses (<10 μg/dl), has not been studied properly yet. The risk of lead poisoning is directly connected not only with an increase in concentration, but also with the duration of the impact of metal. There are a number of possible ways of how exposure of lead reduces male fertility. Lead, most likely, impairs the endocrine profile of regulation, mainly through the axis of the hypothalamus-pituitary testosterone, hereafter reduces the production of sperm in the seminiferous tubules of the testicles. At the same time, it acts as an endocrine destroyer, affecting hormones responsible for the production of sperm. In addition to changes in the reproductive hormone axis and hormonal control of spermatogenesis, the activity of enzymes, such as alkaline phosphatase and potassium-sodium ATP-ase, direct toxic effects on the seminiferous tubules, the exposure time of the metal and its dose affect male infertility. Another problem associated with the reproductive toxicity of lead is determined by the excessive generation of the reactive oxygen species. It is known that the oxidative stress caused by lead is involved in the abnormal functions of spermatozoa and male infertility. The possibility to decrease lead level in the body using a number of methods, such as chelatotherapy, nano-encapsulation, use of N-acetylcysteine is considered. Conclusion. Based on animal studies, it seems to be rational to prescribe the corresponding antioxidants to persons suffering from abnormal parameters of spermatozoa and infertility due to the effects of lead. Antioxidants showed a protective effect on spermatogenesis on animal models and reduced reactive oxygen species in sperm and DNA fragmentation in studies in humans. Although there is no final evidence confirming the use of antioxidant additives in men with low fertility to improve fertility rates, it is believed that due to the low cost and a small number of side effects, antioxidants need to be recommended to men with insufficient fertility

Cadmium salts are among the TOP-20 of the most dangerous compounds for animals in terms of toxicity. At the same time, today there is a paradigm shift in the studies of cadmium effects: in contrast to the acute effects of intoxication, more importance and practical relevance is attained by studying the continued chronic exposure to small cadmium doses (Chronic Low Cd Exposure) which can take place in real environmental conditions of industrially polluted regions and already impacts about 10% of the world population. While the early changes in kidneys and marker parameters of the urinary system under the action of cadmium are being studied quite actively, cadmium effects on other organs and systems in the body are insufficiently investigated. The purpose of the study was to analyse the multiple effects of cadmium on liver function, osteogenesis, haematopoiesis, and haemostasis in animals and humans. Protective mechanisms that reduce cadmium accumulation in hepatocytes compared to renal cells, in particular, the role of cellular transporters of biogenic metal ions (Fe2+, Zn2+, Mn2+, Cu2+), are systematized. Results and discussion. Cadmium mostly uses divalent metal transporter 1 and Zrt/Irt-like transporters, such as ZIP8 and ZIP14. Given the role of liver in the chelation and deposition of cadmium in the form of complexes with metallothioneins and glutathione, the significant potential of chelating and antioxidant hepatoprotectants to reduce negative effects is suggested. The role of exogenous chemical chelators and antioxidants in detoxifying cadmium is supported by the studies of other cadmium-binding molecules (glutathione, polyphenols, anthocyanins). Both direct effects of cadmium on the osteogenesis and calcium metabolism, and indirect effects on osteoblasts and osteoclasts are considered. In particular, current data on cadmium role in the development of endemic disease Itai-Itai in Japan is discussed. Notably, cadmium effect in children has a special hazards and long-term consequences. Data on cadmium role in interfering Ca2+ metabolism, particularly its effects on epithelial calcium channels (TRPV5) and Na-phosphate co-transporters (SLC34A1) are summarized. Conclusion. Current data suggest that chronic effects of cadmium in ultra-low concentrations upon the osteogenesis are even more evident than in renal system. A review of current data on cadmium effects upon the hematopoietic system in animal models is presented. The earliest studies found relation between cadmium and haemoglobin decrease, which could be mediated by interfering with intracellular Fe traffic, and effects on erythropoietin synthesis. Cadmium affected haemostasis and increased platelet aggregation. Animal studies suggest that chronic cadmium toxicity leads to hypercoagulation and increases the risks of thrombosis. Based on the summarized data, it is concluded that the investigating cadmium effects on hematopoiesis and hemostasis is a promising area for further studies of chronic low-dose cadmium exposure