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Lactic acidosis can also be the result of illnesses, medications, poisonings or inborn errors of metabolism that interfere directly with oxygen utilization by cells. [1] The symptoms are generally attributable to the underlying cause, but may include nausea, vomiting, shortness of breath, and generalised weakness.
Pyruvate carboxylase deficiency is an inherited disorder that causes lactic acid to accumulate in the blood. [2] High levels of these substances can damage the body's organs and tissues, particularly in the nervous system. Pyruvate carboxylase deficiency is a rare condition, with an estimated incidence of 1 in 250,000 births worldwide.
Aristolochic acid (contained in herbs in the genus Aristolochia e.g. Aristolochia serpentaria (Virginia snakeroot), Aristolochia reticulata (Texas snakeroot) and in Chinese herbs such as Aristolochia fangchi and Aristolochia manshuriensis [7] (banned in China and withdrawn from Chinese Pharmacopoea 2005; Stephania tetrandra and Magnolia ...
Lactic acid is used as a food preservative, curing agent, and flavoring agent. [51] It is an ingredient in processed foods and is used as a decontaminant during meat processing. [52] Lactic acid is produced commercially by fermentation of carbohydrates such as glucose, sucrose, or lactose, or by chemical synthesis. [51]
It was once believed that lactic acid build-up was the cause of muscle fatigue. [8] The assumption was lactic acid had a "pickling" effect on muscles, inhibiting their ability to contract. Though the impact of lactic acid on performance is now uncertain, it may assist or hinder muscle fatigue.
This theory has been largely rejected, as concentric contractions which also produce lactic acid have been unable to cause DOMS. [5] Additionally, lactic acid is known from multiple studies to return to normal levels within one hour of exercise, and therefore cannot cause the pain that occurs much later.
Lactic acidosis arises from impairment of gluconeogenesis. Lactic acid is generated both in the liver and muscle and is oxidized by NAD + to pyruvic acid and then converted via the gluconeogenic pathway to G6P. Accumulation of G6P inhibits the conversion of lactate to pyruvate. The lactic acid level rises during fasting as glucose falls.
Symptoms may be constant or brought on by an event causing stress, such as an asthma attack, seizure, or infection. Symptoms in the neonatal period include hypotonia, lethargy, vomiting, and tachypnea. As the disease progresses, it causes developmental delay, cognitive disabilities, abnormal development of the face and head, and organ failure. [1]
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