Emergency Medicine International

Review Article

Aluminum Poisoning with Emphasis on Its Mechanism and Treatment of Intoxication

Table 1

Mechanism of aluminum poisoning and its clinical presentations.


Organs	Kidney	Brain	Parathyroid and musculoskeletal	Bone marrow and hematopoiesis	Liver	Lungs

Mechanism of aluminum poisoning	Increasing oxidative stress and lipid peroxidation as well as oxidative stress to DNA and proteins Decreasing GSH content and GSH-Px, GST, and CAT activities Changing renal-tubular p-aminohippuric acid transport, renal-tubular phosphate reabsorption, and sodium water balance impairment Inhibiting Na+/K + ATPase action Increasing free intracellular Fe⁺² resulting in oxidative stress	ROS generation leads to lipid peroxidation, MMP inhibition, ATP reduction, neurotransmitter dysfunction, and neural death Preventing DNA and RNA formation Preventing DNA repair Inhibiting PP2A activity resulting in tau and neurofilament proteins hyperphosphorylation Increasing biosynthesis of the transferrin receptor prevention of ferritin production increase iron in cytoplasmic pools of neurons leading to oxidative stress Corticoneuronal apoptosis through SAPK/JNK pathway Increasing NF-ķβ activation Increasing p53 and BAX resulting in apoptosis Reducing gene expression of neurofilament, tubulin, transferrin receptor, amyloid precursor protein, and neuron-specific enolase Altering expression of RNA polymerase I, oxidative stress, and β-APP secretase Interfering with cellular function Amyloid β accumulation in the brain and theophyllation of tau Increasing free intracellular Fe⁺² resulting in oxidative stress	Reducing parathyroid response to hypocalcemia Inhibiting remodeling and decreasing the number of osteocytes and osteoblasts at higher doses	Inhibiting hemoglobin synthesis	Degeneration in RER that results in a reduction in protein synthesis and change in Ca⁺² levels Swelling of liver cells mitochondria and permeability change in mitochondria membrane Increase ALT and MDA activity up to 4 times Increase proinflammatory cytokines such as TNF-α up to seven times Increase free intracellular Fe⁺² that leads to oxidative stress and anaerobic respiration and decreases ATP production Inhibits Na+/K + ATPase action	Increased PMN influx Minimal interstitial inflammation Type II cell hyperplasia Decrease in alveolar lavageable macrophages
Pathophysiology and clinical manifestations	Reduction in glomerular filtration Changing serum levels of urea, creatinine, and uric acid Nephrotic syndrome Acute renal glomerulonephritis	Memory loss Tremor Jerking movements Diminished coordination Weakness motor movement Lack of curiosity Ataxia Speech disturbances Myoclonic jerks Generalized convulsions Agitation and confusion Grand mal seizures Obtundation Coma Death	Hypothyroidism osteoporosis osteomalacia Decreased bone formation Nonhealing fractures Erosive arthropathy with cysts Spondyloarthropathy Calcium deposition in soft tissue Amyloidosis Chondrocalcinosis	Anisocytosis Poikilocytosis Leptocyte formation Acanthocyte formation Echinocyte formation Stomatocyte formation Target cell formation Microcytic hypochromic anemia	Obesity Type 2 diabetes liver steatosis	Asthma Chronic bronchitis Chronic pneumonia Pulmonary alveolitis COPD Pulmonary fibrosis Alveolar proteinosis Pneumoconiosis Potroom asthma

GSH: glutathione, GSH-Px: glutathione peroxidase, GST: glutathione S-transferase, CAT: catalase, ROS: reactive oxygen species, MMP: mitochondrial membrane potential, PP2A: protein phosphatase 2A, SAPK/JNK: stress-activated protein kinase or c-Jun N-terminal kinase, BAX: B-cell lymphoma- Associated X, β-APP: β-amyloid precursor protein, RER: rough endoplasmic reticulum, ALT: alanine aminotransferase, MDA: malondialdehyde, PMN: polymorphonuclear leukocyte, and COPD: chronic obstructive pulmonary disease.