Liver function tests protein synthesized in the liver. It is the carrier of the copper ion. Its levels is increased in infections, rheumatoid arthritis, pregnancy, non Wilson liver disease and obstructive jaundice. In Wilson disease, the ceruloplasmin level is depressed which lead to copper accumulation in body tissues. AFP is significantly expressed in foetal liver. However, the mechanism that led to the suppression of AFP synthesis in adults is not fully known. Exposure of the liver to cancer-causing agents and arrest of liver maturation in childhood can lead to the rise in AFP. AFP can reach until 400–500 μg/L in hepatocellular carcinoma. AFP
Copper toxicity gastrointestinal distress. Individuals with glucose-6-phosphate deficiency may be at increased risk of hematologic effects of copper. Hemolytic anemia resulting from the treatment of burns with copper compounds is infrequent. Chronic (long-term) copper exposure can damage the liver and kidneys. Mammals have efficient mechanisms to regulate copper stores such that they are generally protected from excess dietary copper levels. Those same protection mechanisms can cause milder symptoms, which are often misdiagnosed as psychiatric disorders. There is a lot of research on the function of the Cu/Zn ratio in neurological, endocrinological, and psychological conditions. Many of the substances that protect us from