Nishie K, Cole RJ, Dorner JW.Toxicity of citreoviridin.
Res Commun Chem Pathol Pharmacol. 1988 Jan;59(1):31-52.
U. S. Department of Agriculture, R. B. Russell Agricultural
Research Center, Athens, GA 30613.
The mycotoxin citreoviridin (CIT) isolated from Penicillium
citreoviride was studied to elucidate the mechanism of its toxic
actions. In CF#1 mice, near lethal doses of CIT decreased motor
activities, body temperature and had cataleptic effects. Male
mice appeared to be more susceptible to CIT and had lower
subcutaneous (sc) LD50 values and longer CIT-induced hypothermia
and hypokinesia. In CIT-treated mice the weights and histology
of liver, kidneys and adrenals were normal one week after sc
treatment, except for the increased adrenal weights in female
mice. Single doses of CIT (sc), given on either day 4 or 5 of
pregnancy (perinidation period), had no adverse effect on the
rates of pregnancy, implantation of ova and embryonal
resorptions in those mice examined on day 12 of pregnancy. CIT
(40 mg/kg ip) produced a brief electro-encephalographic (EEG)
activation, cardiac sinus arrhythmias and tachypnea in the
rabbit. Intravenous (iv) lethal doses of CIT (greater than or
equal to 5 mg/kg) caused an EEG activation followed by high
voltage delta waves, increased the T wave in the
electrocardiogram (ECG) and depressed the respiratory amplitude.
The death caused by iv CIT started with the respiratory arrest,
followed by isoelectric EEG and ECG was the last to stop. In
urethane-anesthetized rabbits CIT decreased the blood pressure,
and in succession it lowered, flattened and inverted the T wave
of ECG suggesting heart ischemia. These observations indicated
that the toxic effects of CIT resulted from respiratory and
cardiovascular failures (apnea, delta EEG waves, sinus
arrhythmia, hypotension) leading to central nervous system
depression due to systemic hypoxia.
PMID: 3258434 |
