Toxic Effects Porphyrins Profile
Porphyrins measured in urine serve as biomarkers of the effects of toxins on the heme biosynthetic pathway. Heme is essential for the proper function of many proteins including oxygen transport, energy production, and detoxification. Patterns of specific porphyrin elevations in urine may serve as functional markers of toxicity from toxic metals (e.g. mercury, lead, or arsenic) or organic chemicals. The Toxic Effects Porphyrins Profile measures seven porphyrins, total porphyrins, and three ratios to help you differentiate heavy metal toxicity, as well as monitor therapy in your patient!

Elevations of the individual porphyrin species can have a number of causes, including heredity and environmental contact. Chronic exposure La toxic metals, Including lead, mercury, arsenic, aluminum, and cadmium often results in organ-specific accumulation that compromises target organ physiological function. Heavy metals impair many aspects of metabolism, while chronic exposure to organic chemicals, such as pesticides, can have deleterious effects on the body's biochemistry and adversely affect cellular function.

Why Evaluate Porphyrins?
Porphyrins are particularly well suited as biomarkers for two reasons. First, the pathway is highly active, so any disturbance tends to cause rapid and relatively large accumulations of intermediates. Second, the enzymes of the porphyrin producing pathway are widely distributed in human tissues and some of them are highly sensitive to the presence of various toxins.

Identify...

• Differentiation of heavy metal toxicity from exposure
• Biochemical damage caused by toxicant exposure
• Mercury's effect in dental patients with amalgams
• Toxicity of patients before and during chelation therapy
• The toxicity of therapeutic drugs

• Multiple chemical sensitivity
• Behavioral and learning disorders
• Immune dysfunctions
• Chronic fatigue
• Neurological and mental/emotional Disorders

Other causes and conditions related to porphyria include:

Genetic Disorders

• Hereditary hyperbilirubinemias
• Bronze baby syndrome
• Erythrohepatic protoporphyria
• Hereditary tyrosinemia

• Diabetes mellitus
• Myocardial infarction
• Hematologic diseases
• Disturbance of iron metabolism

• Infectious diseases
• Liver diseases
• Malignancies
• Other Conditions
• Pregnancy
• Carbohydrate fasting

Figure 1. The Heme Pathway

The highly regulated heme pathway consists of eight enzyme-driven reactions. Reactions begin and end inside the mitochondria, with intervening steps carried out in the cytosol. When porphyrinogens build up, they are easily oxidized to porphyrins that appear in urine. Toxicants like heavy metals and organic xenobiotics bind to one or more enzymes to produce specific patterns of urinary porphyrin elevation. Oxidized porphyrins that accumulate in the body become additional toxicants that cause further tissue degradation. The blockages also slow down the production of the heme-requiring proteins listed at the upper left.

Uroporphyrinogen I is produced in a non-enzymatic reaction that leads to the inactive by-product coproporphyrin I. Some toxicants (especially arsenic) slow the metabolism of Uroporphyrinogen 111, causing diversion to copraporphyrinogen I, so the copra I/III ratio becomes elevated.

Porphyrins Profile Sample Report
In this example, the major intermediates are uroporphyrins I and III and coproporphyrins I and III, as shown by their higher than normal concentrations. Various patterns (Table 1) may appear, indicating specific toxin effects. Indefinite patterns can show overlapping effects of multiple exposure. Whatever the cause, abnormal buildup of intermediates is evidence of toxicity, nutrient deficiency, or genetic enzyme effects causing metabolic impairment.