Mercury is a heavy metal that is extremely toxic. There are three types of it: inorganic, organic, and elemental. Mercury in all its forms has been shown to have harmful effects on living things. It can multiply its concentration from lower to higher trophic levels and accumulate in the body's various tissues. Aquatic organisms bodies have been exposed to mercury mostly through various human activities. The largest source of mercury pollution in the air is thermal power plants that mostly use coal as fuel. It is carried to a body of water after being deposited on the ground surface from the air. The way it enters the food chain is through aquatic plants and animals. Mercury accumulations in the kidney, liver, gills, or gonadal tissues of species that are readily exposed and ingested in aquatic organisms environments. There are possible effects of mercury exposure at both acute and long-term levels. The length of time, the mode of exposure, and the dosage all affect how harmful a substance is. The current study provides information about the harmful effects of mercury in aquatic organisms environments. Even though significant mitigation measures and recommendations were implemented, this assessment provides a comprehensive account of mercury sources and emissions, as well as their destiny and movement across the various environmental compartments. Because of the existing mercury emissions and stability, eating fish still poses a major risk. Aquatic life may be toxically affected by mercury pollution in freshwater environments. Through the food chain, mercury buildup in aquatic organisms can also endanger human health. Aquatic creatures include macroinvertebrates and fish. which people ingest and put their health at serious risk. The effect of mercury on hydrocarbons and how it enters the food chain to reach humans has been identified.
Hemorrhagic insult is a major source of morbidity and mortality in both adults and newborn babies in the developed countries. The mechanisms underlying the non-traumatic rupture of cerebral vessels are not fully clear, but there is strong evidence that stress, which is associated with an increase in arterial blood pressure, plays a crucial role in the development of acute intracranial hemorrhage (ICH), and alterations in cerebral blood flow (CBF) may contribute to the pathogenesis of ICH. The problem is that there are no effective diagnostic methods that allow for a prognosis of risk to be made for the development of ICH. Therefore, quantitative assessment of CBF may significantly advance the underst