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BITTER MELON

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Bitter melon, an herbal, is from the annual plant, Momordica charantia. It is an edible tropical fruit used mostly as a traditional medicine in China, India, and Africa. Parts of the plant used in herbal preparations are from the fruit, leaves, seeds, and seed oil. The main glycosides found in this plant include mormordin and charantin, a hypoglycemic agent.

Specific Substances

    1) African cucumber
    2) Acucurbit
    3) Art pumpkin
    4) Balsam pear
    5) Bitter apple
    6) Bitter cucumber
    7) Bitter gourd
    8) Bitter pear melon
    9) Balsam apple
    10) Cerasee
    11) Carilla cundeamor
    12) Cindeamor
    13) Concombre African
    14) Cundeamor
    15) Karela
    16) Kuguazi
    17) Margose
    18) Momordica charantia L.
    19) Momordica charantia lectin
    20) Momordica muricata
    21) Wild cucumber
    22) CAS 93333-80-3 (Protein, from Momordica charantia seeds)
    23) CONCOMBRE AFRICAIN
    24) GARILLA CUNDEAMOR
    25) MOMORDICA CHARANTIA

Available Forms Sources

    A) FORMS
    1) Herbal preparations of bitter melon are available in dried fruit in tablet form, capsule, fresh juice, tincture, aqueous extract, seed, tea, and a powder form (Duke et al, 2002; Anon, 1999).
    B) SOURCES
    1) Parts of the plant used for medicinal purposes include the fruit, leaves, seeds, and seed oil (Anon, 1999). Commercial bitter melon extracts are available; however, the best form may be 100 milliliters (mL) of decoction (Cunnick & Takemoto, 1993) or 2 ounces of fresh juice. The decoction is made by chopping 100 grams of the fruit and boiling it in 200 mL of water until the volume reduces to 100 mL. Unripe bitter melon is usually available at Asian grocery stores (Cunnick & Takemoto, 1993). Bitter melon is available as a dietary supplement in the United States under the Dietary Supplement Health and Education Act of 1994.
    C) USES
    1) Most commonly, this herbal is used for its antidiabetic properties. Other common uses have included antimicrobial and antifertility. Traditionally, bitter melon has been used a folk remedy for tumors, asthma, skin infections, gastrointestinal disorders, hypertension, and for many other ailments (Duke et al, 2002; Anon, 1999). Complementary and alternative medicine indications include: diabetes mellitus, appetite stimulant (in traditional Chinese medicine), cancer, HIV infection, and gastrointestinal infections (Raman & Lau, 1996; Zhang, 1992). An Ayurvedic herbal preparation of bitter melon has been used for the treatment of increased intraocular pressure (Mistry & Patel, 1991). A less common use of bitter melon has been as an insecticide in tropical countries(Cunnick & Takemoto, 1993).
    2) ANIMAL STUDIES
    a) Chronic treatment with hot water extract of bitter melon decreased the development of mammary tumors in SHN mice, as well as, the development of uterine adenomyosis in mice (Nagasawa et al, 2002).
    b) Treatment with bitter melon extract inhibited aberrant crypt foci in rat colon suggesting that bitter melon may be a chemoprotective agent against colon carcinogenesis (Chiampanichayakul et al, 2001).

Overview

Life Support

    A) This overview assumes that basic life support measures have been instituted.

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) Bitter melon, a herbal derived from the plant Momordica charantia, is mainly a hypoglycemic agent in humans. Components of bitter melon extract appear to have structural similarities to animal insulin. Bitter melon has low clinical toxicity, with some possible gastrointestinal effects and hypoglycemic effects in susceptible persons.
    B) In animals, the principle toxicity is to the liver and reproductive system. These effects have not yet been reported in humans.
    0.2.3) VITAL SIGNS
    A) Constituents of bitter melon have been reported to be hypotensive, although no human data could be found (Duke et al, 2002; Raman & Lau, 1996).
    B) ANIMAL STUDY - Bitter melon and a combination of Maitake mushroom extract lowered the systolic blood pressure in Zucker fatty rats (Talpur et al, 2002).
    0.2.8) GASTROINTESTINAL
    A) Large doses may result in vomiting and diarrhea.
    0.2.20) REPRODUCTIVE
    A) Experiments with isolated components in mice indicate a potential risk in early pregnancy.

Laboratory Monitoring

    A) Plasma levels of the glycoside or any of the plant components are not clinically useful.
    B) Monitor vital signs.
    C) Monitor blood glucose in symptomatic patients. Monitor blood glucose at least hourly, and more frequently if necessary, in patients who develop hypoglycemia.
    D) Monitor for clinical evidence of hypoglycemia (eg, tachycardia, altered mental status, diaphoresis).

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) Treatment is symptomatic and supportive. Most cases of toxicity have involved chronic ingestion; GI decontamination is often not indicated. Administer activated charcoal in symptomatic patients and those with large ingestions or significant coingestants. Patients should be provided with food and encouraged to eat.
    1) ACTIVATED CHARCOAL: Administer charcoal as a slurry (240 mL water/30 g charcoal). Usual dose: 25 to 100 g in adults/adolescents, 25 to 50 g in children (1 to 12 years), and 1 g/kg in infants less than 1 year old.
    C) Treat patients who develop laboratory evidence of hypoglycemia (blood glucose less than 60 milligrams/deciliter) or significant clinical effects with food and IV dextrose.
    D) ADULTS - 50 milliliters of 50% dextrose IV push and repeat as needed to achieve a blood glucose of 100 milligrams/deciliter.
    E) CHILDREN - 0.5 to 1 gram/kilogram (2 to 4 milliliters/kilogram of 25% dextrose) repeated as needed to achieve a blood glucose of 100 milligrams/deciliter.
    F) Prophylactic dextrose administration is not recommended in patients who do not become hypoglycemic.
    G) MONITOR BLOOD GLUCOSE and vital signs hourly; monitor for clinical evidence of hypoglycemia. Patients who develop hypoglycemia should be admitted and monitored.

Range Of Toxicity

    A) Neither a toxic nor a standardized dose has been established. Two children experienced hypoglycemic seizures after ingestion of a water extract of the plant leaves and vines.

Clinical Effects

Summary Of Exposure

    A) Bitter melon, a herbal derived from the plant Momordica charantia, is mainly a hypoglycemic agent in humans. Components of bitter melon extract appear to have structural similarities to animal insulin. Bitter melon has low clinical toxicity, with some possible gastrointestinal effects and hypoglycemic effects in susceptible persons.
    B) In animals, the principle toxicity is to the liver and reproductive system. These effects have not yet been reported in humans.

Vital Signs

    3.3.1) SUMMARY
    A) Constituents of bitter melon have been reported to be hypotensive, although no human data could be found (Duke et al, 2002; Raman & Lau, 1996).
    B) ANIMAL STUDY - Bitter melon and a combination of Maitake mushroom extract lowered the systolic blood pressure in Zucker fatty rats (Talpur et al, 2002).

Neurologic

    3.7.2) CLINICAL EFFECTS
    A) HEADACHE
    1) Some diabetic patients have complained of headache while taking bitter melon seeds (Grover & Gupta, 1990). Favism, with headache, fever, abdominal pain and coma, is reportedly induced by vicine a toxic seed constituent (Anon, 1999; Cunnick & Takemoto, 1993; Raman & Lau, 1996).

Gastrointestinal

    3.8.1) SUMMARY
    A) Large doses may result in vomiting and diarrhea.
    3.8.2) CLINICAL EFFECTS
    A) DIARRHEA
    1) Abdominal pain, vomiting and diarrhea have been reported following ingestion of the juice or dried juice powder (Raman & Lau, 1996; Anon, 1999). A saponic glycoside yielding leaterin (a cucurbitacin), is contained in the seeds and wall of the fruit, which causes vomiting and diarrhea (Cunnick & Takemoto, 1993).

Hepatic

    3.9.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) Administration of bitter melon fruit juice or seed extract to rats resulted in a significant increase in serum gamma-glutamyl transferase concentrations (p < 0.0001) and in serum alkaline phosphatase concentrations (p<0.01 with fruit juice; p < 0.001 with seed extract) compared with controls. Daily doses of 1 milliliter/kilogram were administered orally under light ether anesthesia. No consistent histopathological changes in the liver were found (Tennekoon et al, 1994).
    2) The Koimidori variety of bitter melon was shown to exhibit liver triglyceride lowering in rats that had bitter melon in their diets (Senanayake et al, 2004).

Genitourinary

    3.10.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) TESTIS DISORDER
    a) Oral administration of karela (bitter melon) fruit extract (1.75 grams/day for 60 days) to male dogs resulted in testicular lesions and mass atrophy of spermatogenic elements. Lowered spermatogenesis was noted. Serum enzymes were normal, implying that an infertility state was induced without altering general metabolic activity (Dixit et al, 1978)

Hematologic

    3.13.2) CLINICAL EFFECTS
    A) HEMATOLOGY FINDING
    1) An in-vitro study using human plasma demonstrated the prolongation of activated partial thromboplastin time by Momordica charantia trypsin inhibitor-II. No actual human cases of coagulation disorders have been reported (Hayashi et al, 1994)

Dermatologic

    3.14.2) CLINICAL EFFECTS
    A) SKIN FINDING
    1) WITH POISONING/EXPOSURE
    a) LACK OF EFFECT
    1) No topical contact allergy nor irritation was reported following contact with bitter melon leaf juice (Duke et al, 2002).

Endocrine

    3.16.2) CLINICAL EFFECTS
    A) HYPOGLYCEMIA
    1) Due to the clinical effects of this plant on reducing blood sugar, susceptible individuals may experience hypoglycemia with large doses or when taken on an empty stomach (Anon, 1999). Limited studies have shown reduction in fasting blood glucose and improvement in glucose tolerance following acute therapeutic administration(Ahmad et al, 1999; Raman & Lau, 1996; William et al, 1993; Grover & Gupta, 1990). Reduced blood glucose concentrations were reported during a 50 gram oral glucose tolerance test in diabetic patients following ingestion of a water-soluble extract or juice of the fruit (Welihinda et al, 1986a; Leatherdale et al, 1981).
    2) In animal studies, bitter melon did not affect the blood glucose of normal animals, just those animals with type II diabetes and hyperinsulinemia. Animals were affected in a dose-dependent manner (Miura et al, 2001). When cholesterol was included in the diet of rats, the hypoglycemic effect of bitter melon was diminished (Jayasooriya et al, 2000).
    3) CASE REPORTS - Hypoglycemia coma was induced in 2 small children ages 3 and 4 years following ingestion of a water extract of Momordica charantia leaves and vines. Tea had been administered early in the morning before any other food had been consumed. Between 1 and 2 hours after ingestion, the children experienced seizures followed by coma. Blood glucose was approximately 1 millimolar (mM) (normal range 3.8 to 5.5 mM). Both patients recovered (Raman & Lau, 1996).
    3.16.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) HYPOGLYCEMIA
    a) Charantin, a mixture of sitosterol and stigmastadienol glucosides, has been isolated from bitter melon and shown to produce a gradual and significant fall in blood sugar in animals. Pancreatectomy reduced, but did not abolish this effect of charantin. Vicine has been isolated from seeds and produced a hypoglycemic response in rats with intraperitoneal administration. Cerasee tea made from bitter melon vines lowered basal glucose concentrations and improved glucose tolerance in normal mice (Raman & Lau, 1996) . Treatment of streptozotocin-induced diabetic mice with bitter melon juice produced a 30% to 50% reduction in blood glucose concentration after 10 weeks of daily feeding (Raza et al, 1996).
    b) Rats that were fed a high fat diet supplemented with freeze-dried bitter melon juice had an improvement in oral glucose tolerance (Chen et al, 2003).
    c) THYROXIN DECREASED
    1) In mice studies, alcoholic extracts of Momordica charantia (400 and 500 mg/kg body weight) given orally daily for 15 days resulted in decreased concentrations of T3 and T4 and enhanced hepatic lipid peroxidation with a concurrent decrease in catalase activity. The study results indicated a thyroid inhibitory effect of this plant. Lower doses (less than 400 mg/kg) did not have thyroid inhibitory effects (Panda & Kar, 2000).

Immunologic

    3.19.2) CLINICAL EFFECTS
    A) IMMUNE SYSTEM FINDING
    1) A crude extract from bitter melon fruit was shown to be cytotoxic to normal human lymphocytes in vitro. The whole fruit was homogenized, filtered, and centrifuged. The supernatant was precipitated, redissolved, and dialyzed, forming a crude extract. The extract was heat-stable but trypsin-sensitive and unstable over time, losing its cytotoxic activity after 6 months storage at 0 degrees C. Normal human lymphocytes from healthy donors were compared with leukemia cell lines. The LD50 for normal cells was over twice that of the leukemic lymphocytic cell lines. While the cytostatic effects in myeloma derived beta cells was shown with 60 micrograms/milliliter (mcg/mL), the cytotoxic dose was 140 mcg/mL, and agglutination of cells occurred at 300 mcg/mL. The effects took only 2 hours to manifest, but were not due to momordin from the seeds (Takemoto et al, 1982).
    3.19.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) IMMUNE SYSTEM DISORDER
    a) The proteins alpha- and beta-momorcharin obtained from bitter melon seeds have been shown to suppress immune responses in vitro and in vivo. In cell cultures of mouse splenocytes the response to several mitogens was inhibited dose-dependently. Cytotoxic lymphocyte response and lymphoproliferation induced by alloantigens were greatly reduced by the momorcharins in vitro. Macrophage phagocytic and cytostatic activities were likewise diminished. The injection of nontoxic amounts of these proteins in living mice depressed antibody formation and delayed hypersensitivity response, as well as macrophage migration. The immune suppressive effects of the two momorcharins are similar and potent, but the target site(s) on cells have not been identified (Leung et al, 1987) .

Reproductive

    3.20.1) SUMMARY
    A) Experiments with isolated components in mice indicate a potential risk in early pregnancy.
    3.20.2) TERATOGENICITY
    A) ANIMAL STUDIES
    1) Momorcharins found in bitter melon seeds are teratogenic in cultured mouse embryos at the early organogenesis stage. Morphological abnormalities of the head, trunk, and limbs have been observed. Teratogenic action is most likely mediated through a harmful effect on the visceral yolk sac (Ng et al, 1992; Chan et al, 1986).
    2) Intraperitoneal injection of an extract of bitter melon into pregnant rats for 10 days beginning on the day of mating was associated with a 54% reduction of fetal weight compared with controls. Delaying the injection to start 3 days after mating was associated with an 8% reduction (West et al, 1971).
    3.20.3) EFFECTS IN PREGNANCY
    A) HUMANS
    1) Bitter melon has known reproductive system toxicities; it may induce uterine bleeding and contractions or abortion induction (Anon, 1999). Alpha-trichosanthine and beta-momorchin in bitter melons seeds are abortifacient (Duke et al, 2002). Bitter melon appears to be effective as an abortifacient in all stages of pregnancy, with the mechanism of action resembling that of ergot alkaloids (Zhang, 1992).
    B) ANIMAL STUDIES
    1) ABORTION
    a) The glycoproteins alpha- and beta-momorcharin, isolated from the seeds of bitter melon, induce mid-term abortion and terminate early pregnancy in mice (Ng et al, 1992; Chan et al, 1986).
    b) Proteins capable of inducing abortions (alpha and beta momorcharins) and necrosis of placental trophoblasts have been isolated from Momordica charantia seeds. Similar proteins may occur in the leaves. Uterine bleeding has been induced in pregnant rats given karela juice (6 mL/kg) orally (Zhang, 1992).
    c) When alpha- and beta-momorcharins were administered (0.1 mg/25 grams body weight) to mice pregnant for 4 and 6 days, abortions were noted in 67% and 60%, respectively. Twice this dose was required to induce abortions in mice pregnant for 1 to 3 days (Ng et al, 1994).
    GROWTH RETARDED
    d) Fetal growth retardation, probably mediated by hypoglycemic activity of bitter melon extract (administered as 1 mL/100 g/day or 2 mL/100 g/day), has been reported in pregnant rats administered the extract during mid (days 8-16) gestation. Also reported were vaginal bleeding (dose-related), resorption of fetuses, post-implantation losses, small for dates fetuses(Fernandopulle & Ratnasooriya, 1999)

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) Plasma levels of the glycoside or any of the plant components are not clinically useful.
    B) Monitor vital signs.
    C) Monitor blood glucose in symptomatic patients. Monitor blood glucose at least hourly, and more frequently if necessary, in patients who develop hypoglycemia.
    D) Monitor for clinical evidence of hypoglycemia (eg, tachycardia, altered mental status, diaphoresis).
    4.1.2) SERUM/BLOOD
    A) URINALYSIS
    1) False negative glycosuria appeared to occur when urine was tested for glucose by glucose oxidase reagent strips in patients receiving 100 grams of bitter melon pulverized fresh fruit daily for 2 weeks. The mechanism suggested, for false negative urine glucose tests, was excretion of a substance that keeps the indicator dye in the glucose oxidase strips and the alkaline copper salts in a reduced state(Kirti et al, 1982)

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Monitoring

    A) Plasma levels of the glycoside or any of the plant components are not clinically useful.
    B) Monitor vital signs.
    C) Monitor blood glucose in symptomatic patients. Monitor blood glucose at least hourly, and more frequently if necessary, in patients who develop hypoglycemia.
    D) Monitor for clinical evidence of hypoglycemia (eg, tachycardia, altered mental status, diaphoresis).

Oral Exposure

    6.5.1) PREVENTION OF ABSORPTION/PREHOSPITAL
    A) SUMMARY - Most cases of toxicity reported have involved chronic ingestion of bitter melon. Gastrointestinal decontamination is generally not indicated. Consider activated charcoal in symptomatic patients or those with large ingestions or significant coingestants.
    6.5.2) PREVENTION OF ABSORPTION
    A) Most cases of toxicity have involved chronic ingestion; GI decontamination is often not indicated. Administer activated charcoal in symptomatic patients and those with large ingestions or significant coingestants.
    B) ACTIVATED CHARCOAL
    a) CHARCOAL ADMINISTRATION
    1) Consider administration of activated charcoal after a potentially toxic ingestion (Chyka et al, 2005). Administer charcoal as an aqueous slurry; most effective when administered within one hour of ingestion.
    a) CHARCOAL DOSE
    1) Use a minimum of 240 milliliters of water per 30 grams charcoal (FDA, 1985). Optimum dose not established; usual dose is 25 to 100 grams in adults and adolescents; 25 to 50 grams in children aged 1 to 12 years (or 0.5 to 1 gram/kilogram body weight) ; and 0.5 to 1 gram/kilogram in infants up to 1 year old (Chyka et al, 2005).
    a) Routine use of a cathartic with activated charcoal is NOT recommended as there is no evidence that cathartics reduce drug absorption and cathartics are known to cause adverse effects such as nausea, vomiting, abdominal cramps, electrolyte imbalances and occasionally hypotension (None Listed, 2004).
    2) ADVERSE EFFECTS/CONTRAINDICATIONS
    a) Complications: emesis, aspiration (Chyka et al, 2005). Aspiration may be complicated by acute respiratory failure, ARDS, bronchiolitis obliterans or chronic lung disease (Golej et al, 2001; Graff et al, 2002; Pollack et al, 1981; Harris & Filandrinos, 1993; Elliot et al, 1989; Rau et al, 1988; Golej et al, 2001; Graff et al, 2002). Refer to the ACTIVATED CHARCOAL/TREATMENT management for further information.
    b) Contraindications: unprotected airway (increases risk/severity of aspiration) , nonfunctioning gastrointestinal tract, uncontrolled vomiting, and ingestion of most hydrocarbons (Chyka et al, 2005).
    6.5.3) TREATMENT
    A) SUPPORT
    1) Treatment is symptomatic and supportive. Toxicity is minimal, with abdominal pain, vomiting and diarrhea expected. Hypoglycemia may develop following an overdose. Patients should be provided with food and encouraged to eat.
    B) HYPOGLYCEMIA
    1) DEXTROSE
    a) Treat patients who develop laboratory evidence of hypoglycemia (blood glucose less than 60 milligrams/deciliter) or clinical signs of hypoglycemia with food and IV dextrose.
    b) DOSE
    1) ADULT
    a) ORAL FEEDING - In an awake and alert patient, the most effective means of maintaining euglycemia is with adequate oral caloric intake.
    b) BOLUS - the administration of 25 grams dextrose solution will correct the majority of acute hypoglycemic states in patients unable to receive adequate calories orally. This dose may need to be repeated in patients with profound hypoglycemia.
    c) INFUSION - Initiation of continuous intravenous infusions may be necessary in patients with recurrent hypoglycemia unable to receive adequate calories orally. Titrate to maintain blood glucose above 100 milligrams/deciliter.
    d) PEDIATRIC
    1) ORAL FEEDING - In an awake and alert patient, the most effective means of maintaining euglycemia is with adequate oral caloric intake.
    2) BOLUS - 0.5 to 1 gram/kilogram intravenously, usually administered as D25W (2 to 4 milliliters/kilogram/dose) given over 1 to 2 minutes in patients unable to receive adequate calories orally.
    3) D50W (1 to 2 milliliters/kilogram/dose) may be used for children greater than 5 years and D10W for preterm infants.
    4) INFUSION - Initiation of continuous intravenous infusion may be necessary in patients with recurrent hypoglycemia unable to receive adequate calories orally. Titrate to maintain blood glucose above 100 milligrams/deciliter.
    5) Prophylactic dextrose administration is not recommended in patients who do not become hypoglycemic.
    C) MONITORING OF PATIENT
    1) FLUID/ELECTROLYTES
    a) MONITOR FLUID and ELECTROLYTE BALANCE - Potassium supplementation may be needed.

Range Of Toxicity

Summary

    A) Neither a toxic nor a standardized dose has been established. Two children experienced hypoglycemic seizures after ingestion of a water extract of the plant leaves and vines.

Therapeutic Dose

    7.2.1) ADULT
    A) DISEASE STATE
    1) DIABETES MELLITUS
    a) IMPORTANT NOTE: Dosing of herbal preparations is highly dependent on a variety of factors, such as growing and harvesting conditions, plant parts and extraction methods used, and the dosage form chosen by the manufacturers. Standardization to single constituent markers has proven unreliable. Since no official standards have been established to date to regulate the production of herbal medicines in the United States, dosage ranges must be employed as guidelines.
    b) Fresh juice, oral: 50 to 100 milliliters daily (Duke et al, 2002; Welihinda et al, 1986a; Leatherdale et al, 1981).
    c) Aqueous extract, oral: 100 milliliters daily (Srivastava et al, 1993)
    d) Powder of dried fruit: 5 grams three times daily(Srivastava et al, 1993)
    e) One (500 milligram) capsule three times daily with 150 milligrams extract containing 2.5% bitter principles(Duke et al, 2002)
    f) 5 milliliters of tincture two to three times daily (Duke et al, 2002)
    g) Administration is via the oral or rectal route (Zhang, 1992). Bitter melon is supplied as dried fruit in tablet or capsule form, extract, fruit, juice, seed or tea.
    7.2.2) PEDIATRIC
    A) DISEASE STATE
    1) Pediatric dosing is not available.

Minimum Lethal Exposure

    A) ANIMAL DATA
    1) Chronic oral dosing in the order of 6 milliliters/kilogram body weight of karela juice has been shown to be fatal in animal studies, with pregnant females most susceptible (Raman & Lau, 1996).

Maximum Tolerated Exposure

    A) PEDIATRIC
    1) Two children, aged 3 and 4 years old, developed hypoglycemic seizures 1 to 2 hours after the ingestion of a water extract of Momordica charantia leaves and vines. Both children recovered after treatment (Raman & Lau, 1996).
    2) Gastrointestinal toxicity has been reported in children due to the red arils (covering around bitter melon seeds). Vomiting, diarrhea, and an unconfirmed death has been reported in one child given the juice(Anon, 1999).

Toxicity Information

    7.7.1) TOXICITY VALUES
    A) MOMORDICA CHARANTIA LINN., EXTRACT
    1) LD50- (INTRAPERITONEAL)MOUSE:
    a) 681 mg/kg (RTECS, 2003)
    B) MOMORDICA CHARANTIA LINN., FRUIT EXTRACT
    1) LD50- (INTRAPERITONEAL)MOUSE:
    a) 681 mg/kg (RTECS, 2003)
    C) PROTEIN, FROM MOMORDICA CHARANTIA SEEDS
    1) LD50- (INTRAPERITONEAL)MOUSE:
    a) 3160 mcg/kg (RTECS, 2003)

Pharmacology Toxicology

Pharmacologic Mechanism

    A) ANTIVIRAL EFFECTS
    1) Momordica anti-HIV protein of 30 kD (MAP 30) found in bitter melon seeds and fruits has antiviral activity against the human immunodeficiency virus (HIV). MAP30 inhibits infection by HIV type 1 in T-lymphocytes and monocytes and replication of the virus in cells already infected. The antiviral actions of MAP30 include an in vitro RNA N-glycosidase activity that cleaves the link between a ribose and a purine in 28S rRNA, DNA topological inactivation activity that renders viral and plasmid DNA topological inactivation activity that renders viral and plasmid DNA topologically inactive, and inhibition of HIV type 1 integrase (De Clercq, 2000; Lee-Huang et al, 1995).
    2) Momordica charantia inhibits HIV syncythial formation (Zhang, 1992).

References

General Bibliography

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