PIX-FAGI SPRAY

Indications

• Antioxidant support
• Anti-inflammatory effects
• Nutritional supplement

Dosage

Children: Refer to herbal medicine guidelines for specific dosing recommendations, as there is no standard dosage established for beech.

Adults: Refer to herbal medicine guidelines for specific dosing recommendations, as there is no standard dosage established for beech.

Mechanism of action

The exact mechanism of action of beech is not well characterized in scientific literature. However, compounds found in beech leaves may exert antioxidant effects by scavenging free radicals, thereby reducing oxidative stress. Additionally, the presence of flavonoids may contribute to anti-inflammatory effects by inhibiting pro-inflammatory cytokines.

Pharmacodynamics

Beech demonstrates potential pharmacological activities, primarily attributed to its phytochemical constituents, including flavonoids and tannins. These compounds may modulate inflammation and oxidative stress, contributing to overall health benefits. However, comprehensive studies are lacking to firmly establish the pharmacodynamics of beech in clinical settings.

Pharmacokinetics

The pharmacokinetics of beech have not been extensively studied. Generally, the absorption, distribution, metabolism, and excretion of herbal constituents can vary widely depending on the specific compounds present. Further research is needed to elucidate the pharmacokinetic properties of beech extracts.

Pregnancy

Insufficient data regarding safety during pregnancy. It is advisable to avoid use unless prescribed by a healthcare professional.

Breast-feeding

Insufficient data regarding safety during breastfeeding. Caution is advised and consultation with a healthcare professional is recommended.

Storage

Store in a cool, dry place away from direct sunlight. Keep out of reach of children.

Dosage

Children: Refer to the BNF for Children for dosing guidelines related to methanol poisoning in paediatric patients.

Adults: For methanol poisoning, treatment typically involves the administration of fomepizole or ethanol as antidotes, alongside supportive care. Refer to the BNF for specific dosing guidelines.

Mechanism of action

Methanol is metabolized primarily by alcohol dehydrogenase to formaldehyde, which is further oxidized to formate. These metabolites, particularly formate, are responsible for the toxic effects associated with methanol poisoning, including metabolic acidosis and visual impairment. Individual susceptibility to methanol toxicity may vary based on metabolic pathways involving folic acid and the rate of formate metabolism.

Pharmacodynamics

Methanol toxicity is characterized by a latent period where initial symptoms may not appear until hours after ingestion. The accumulation of formate leads to metabolic acidosis, which can cause serious physiological disturbances. Methanol's effects can be exacerbated by individual differences in metabolic capacity and the presence of concurrent conditions affecting folic acid metabolism.

Pharmacokinetics

Methanol is rapidly absorbed from the gastrointestinal tract, with peak blood concentrations occurring within 30 to 60 minutes after ingestion. It is metabolized primarily in the liver, where it undergoes oxidation to formaldehyde and then to formate, which is further metabolized to carbon dioxide. The elimination half-life of methanol varies depending on the rate of metabolism, which can be influenced by factors such as liver function and the presence of other substances.

Adverse effects

• metabolic acidosis
• visual impairment
• nausea
• vomiting
• headache
• dizziness
• confusion
• respiratory distress

Precautions

• Monitor for signs of metabolic acidosis
• Assess individual susceptibility to methanol toxicity
• Avoid concurrent use with other substances that may exacerbate toxicity

Pregnancy

Methanol should be avoided during pregnancy due to potential risks to the fetus, including developmental toxicity.

Breast-feeding

Caution is advised as methanol can be excreted in breast milk and may affect the nursing infant.

Storage

Store in a cool, dry place away from heat and direct sunlight. Keep out of reach of children.

Mechanism of action

... The metabolic mechanisms of methanol toxicity /are/ reviewed. ... It is noted that the most severe toxicity occurs many hours following peak blood and tissue methanol concentrations so that these do not necessarily provide an accurate indication of toxicity. Individual differences are seen both in this latent period and in individual susceptibility to methanol. This susceptibility may depend on the activity of folic acid requiring metabolic reactions involved in formate metabolism, formate being an intermediate produced during methanol oxidation and responsible for many toxic effects of methanol. Studies of the characteristics of methanol poisoning in non-primates and monkeys are examined. Despite the ingestion of lethal doses of methanol, non-primates generally do not develop significant metabolic acidosis nor impairment of vision, and no consistent histopathology has been demonstrated in these species. In monkeys, results suggest that the latent period represents a period of compensated metabolic acidosis; when compensatory mechanisms are exhausted, blood pH begins to drop. Formate accumulates and produces acidosis in the methanol poisoned monkey, but not in the rat, apparently due to a slower rate of formate metabolism to carbon dioxide in the monkey. ... Studies demonstrating the role of alcohol dehydrogenase in methanol metabolism in the monkey are reported; however, the catalase/peroxidative system which participates in methanol metabolism in rats apparently does not function in the monkey. Formaldehyde and formate metabolism are also examined. The regulation of the rate of formate metabolism is governed by regulation of the hepatic tetrahydrofolate concentrations. ... Further research is needed to determine what step or process it is which places the primate at a distinct liability in the metabolic disposition of one carbon moieties. Methanol toxicity is observed in monkeys and humans but is not seen in rats or mice. The expression of methanol poisoning is related to the ability of an animal to metabolize formate to carbon dioxide. Since the rate of formate oxidation is related to hepatic tetrahydrofolate content and the activites of folate dependent enzymes, studies were designed to determine hepatic concentrations of hepatic tetrahydrofolate and activites of folate dependent enzymes of human liver and livers of species considered insensitive to methanol poisoning. An excellent correlation between hepatic tetrahydrofolate and maximal rates of formate oxidation has been observed. In human liver, levels were only 50% of those observed for rat liver and similar to those found in monkey liver. Total folate was also lower (60% decreased) in human liver than that found in rat or monkey liver. Interestingly, mouse liver contains much higher hepatic tetrahydrofolate and total folate than rat or monkey liver. This is consistent with higher formate oxidation rates in this species. A second important observation has been made. 10-Formyltetrahydrofolate dehydrogenase activity, the enzyme catalyzing the final step of formate oxidation to carbon dioxide, was markedly reduced in both monkey and human liver. Thus, two mechanisms may be operative in explaining low formate oxidation in species susceptible to methanol toxicity, low hepatic tetahydrofolate levels and reduced hepatic 10-formyltetrahydrofolate dehydrogenase activity. Formic acid, the toxic metabolite of methanol, has been hypothesized to produce retinal and optic nerve toxicity by disrupting mitochondrial energy production. It has been shown in vitro to inhibit the activity of cytochrome oxidase, a vital component of the mitochondrial electron transport chain involved in ATP synthesis. Inhibition occurs subsequent to the binding of formic acid to the ferric heme iron of cytochrome oxidase, and the apparent inhibition constant is between 5 and 30 mM. Concentrations of formate present in the blood and tissues of methanol-intoxicated humans, non-human primates and rodent m