Helenalin

Danger

H301 (100%): Toxic if swallowed [Danger Acute toxicity, oral]

P264, P270, P301+P316, P321, P330, P405, and P501 (click each P-code to see the statement)

The GHS information provided by 1 company from 1 notification to the ECHA C&L Inventory.

Causes seizures at lethal doses in mice; Intraperitoneal LD50 (mouse) = 10 mg/kg; [RTECS] Especially toxic in flowering stage; may cause paralysis of voluntary and cardiac musculature and fatal gastroenteritis; Emergency treatment: Plants- sesquiterpene lactones; Sesquiterpene lactones are in many plants. They cause toxicity mainly in livestock that eat the plants. Human poisoning cases are extremely rare. Possible symptoms after ingestion include irritation of mucous membranes, dyspnea, pulmonary hemorrhage, tremors, seizures, abdominal pain, and liver injury. [HSDB] Sesquiterpene lactones are a common cause of allergic dermatitis in florists. See Sesquiterpene lactones.

INTENSELY POISONOUS, CAPABLE OF CAUSING PARALYSIS OF VOLUNTARY & CARDIAC MUSCULATURE & FATAL GASTROENTERITIS.

DOGS TOLERATED RAPID IV INJECTIONS OF 0.3% HELENALIN OR CRUDE 50% ETHANOL EXTRACT OF HELENIUM MICROCEPHALUM AT A MAXIMUM CUMULATIVE DOSE OF 90 MG HELENALIN/KG OR A MAXIMUM OF 10 G PLANT/KG. THE PHARMACODYNAMIC RESPONSES WERE AN INITIAL CHOLINERGIC EFFECT, A NICOTINIC EFFECT, STIMULATION OF THE RESPIRATORY & CENTRAL NERVOUS SYSTEMS, & PROGRESSIVE CARDIAC FAILURE.

THE MODE OF ACTION OF HELENALIN AS A PROTEIN SYNTHESIS INHIBITOR IN P-388 LYMPHOCYTIC LEUKEMIA CELLS WAS INVESTIGATED IN CRUDE LYSATES OF THE CELLS. THERE WAS A 4-MIN LAG AFTER THE ADDITION OF DRUG BEFORE INHIBITION OF PROTEIN SYNTHESIS OCCURRED. BOTH DRUGS ALLOWED RUN-OFF OF PREFORMED POLYSOMES BUT DID INHIBIT THE FORMATION OF 80 S INITIATION COMPLEX, SUGGESTING A PREFERENTIAL INHIBITION OF GREATER THAN OR EQUAL TO INITIATION REACTIONS.

HELENALIN WAS CAPABLE OF ALKYLATING THE THIOL GROUP OF REDUCED GLUTATHIONE & L-CYSTEINE IN VITRO. HELENALIN WAS ACTIVE AGAINST EHRLICH ASCITES & WALDER 256 ASCITES CARCINOSARCOMA IN VIVO & HAD CYTOTOXIC ACTIVITY AGAINST H.EP-2 TUMOR CELLS IN VITRO.

Anti-inflammatory agents that are non-steroidal in nature. In addition to anti-inflammatory actions, they have analgesic, antipyretic, and platelet-inhibitory actions. They act by blocking the synthesis of prostaglandins by inhibiting cyclooxygenase, which converts arachidonic acid to cyclic endoperoxides, precursors of prostaglandins. Inhibition of prostaglandin synthesis accounts for their analgesic, antipyretic, and platelet-inhibitory actions; other mechanisms may contribute to their anti-inflammatory effects.

Agents obtained from higher plants that have demonstrable cytostatic or antineoplastic activity.

Agents that have a strengthening effect on the heart or that can increase cardiac output. They may be CARDIAC GLYCOSIDES; SYMPATHOMIMETICS; or other drugs. They are used after MYOCARDIAL INFARCT; CARDIAC SURGICAL PROCEDURES; in SHOCK; or in congestive heart failure (HEART FAILURE).

Drugs or agents which antagonize or impair any mechanism leading to blood platelet aggregation, whether during the phases of activation and shape change or following the dense-granule release reaction and stimulation of the prostaglandin-thromboxane system.