나트륨 부티르산

Warning

H302 (16.7%): Harmful if swallowed [Warning Acute toxicity, oral]；H315 (100%): Causes skin irritation [Warning Skin corrosion/irritation]；H319 (100%): Causes serious eye irritation [Warning Serious eye damage/eye irritation]；H335 (88.9%): May cause respiratory irritation [Warning Specific target organ toxicity, single exposure; Respiratory tract irritation]；H341 (33.3%): Suspected of causing genetic defects [Warning Germ cell mutagenicity]

P203, P261, P264, P264+P265, P270, P271, P280, P301+P317, P302+P352, P304+P340, P305+P351+P338, P318, P319, P321, P330, P332+P317, P337+P317, P362+P364, P403+P233, P405, and P501 (click each P-code to see the statement)

Aggregated GHS information provided per 18 reports by companies from 14 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.；Information may vary between notifications depending on impurities, additives, and other factors. The percentage value in parenthesis indicates the notified classification ratio from companies that provide hazard codes. Only hazard codes with percentage values above 10% are shown. For more detailed information, please visit ECHA C&L website.

Chemical: Butanoic acid, sodium salt

Butanoic acid, sodium salt: Does not have an individual approval but may be used as a component in a product covered by a group standard. It is not approved for use as a chemical in its own right.

SODIUM BUTYRATE INHIBITED INITIATION OF VIRAL AND CELLULAR DNA REPLICATION IN POLYOMA VIRUS-INFECTED MOUSE KIDNEY CELLS.

24 HR AFTER TREATMENT OF FRIEND ERYTHROLEUKEMIA CELLS WITH MILLIMOLAR CONCN OF SODIUM BUTYRATE, THE CHROMATIN HISTONES HAD BECOME HYPERACETYLATED. DURING THIS SAME TIME PERIOD, THE BUTYRATE-TREATED FRIEND CELLS ACCUMULATED A POPULATION OF APPROX 38% NEW RNA TRANSCRIPTS SYNTHESIZED FROM UNIQUE SEQUENCES OF MOUSE DNA.

F9 mouse teratocarcinoma stem cells differentiate into parietal endoderm cells in the presence of retinoic acid, dibutyryl cyclic AMP, and theophylline. When F9 cells are exposed to 2-5 mM sodium butyrate plus retinoic acid, dibutyryl cyclic AMP, and theophylline, they fail to differentiate. Butyrate inhibits differentiation only when added within 8 hr after retinoic acid addition. Thus an early event in retinoid action on F9 cells is butyrate-sensitive. Butyrate inhibits histone deacetylation in F9 cells, and this could be the mechanism by which butyrate inhibits differentiation.

Sodium butyrate treatment enhanced the development of colonic neoplasia and was associated with increased fecal butyric acid concentrations in rats given parenteral administration of 1,2-dimethylhydrazine.

Inhibitors of DNA polymerase efficiently inhibit initiator induced amplification of SV40 DNA sequences in the SV40 transformed Chinese hamster cell line CO631. Sodium butyrate inhibits DNA synthesis by histone modification.

Since cancer may be regarded as a disease of differentiation and sodium butyrate induces differentiation of malignant cells in vitro, a study of the clinical pharmacology of sodium butyrate was undertaken. Nine patients with acute myeloid (n= 1), acute monocytic (n= 1), acute myelomonocytic (n= 6) and acute undifferentiated (n= 1) leukemia were treated. Their median age was 52 (range, 27-78) years. Six of the nine patients were pretreated with cytostatic agents. Sodium butyrate was administered iv at a dosage of 500 mg/kg/day as continuous infusion over 10 days. A sensitive and reproducible high-performance liquid chromatographic separation was developed after derivatization of sodium butyrate with 2,4'-dibromoacetophenone employing crown ether catalysts. Plasma concentrations and urinary excretion of sodium butyrate were monitored during the 10 days of continous infusion and for 2 days thereafter. During infusion, plasma concentrations increased 6-fold over the endogenous butyrate level and reached 39-59 uM. The area under the curve of the exogenous butyrate was 384 + or - 50 uM X day (mean + or - standard deviation). After the end of infusion, concentrations declined rapidly with a half-life of 6.1 + or - 1.4 min, and reached pretreatment values within 1 hr. The total clearance rate was 83 + or - 12 ml/kg/min and the volume of distribution 738 + or - 245 ml/kg. The excreted amounts of butyrate in the urine were minmal as compared to the infused dose. Although excretion by other organs was not ruled out, it is suggested that the infused sodium butyrate was rapidly metabolized. A significant increase in peripheral blast cells was observed, whereas bone marrow cytologies before and after treatment did not reveal a significant change in blasts. Differential counts of peripheral white blood cells did not show significantly changes. No toxicity was encountered. The apparent lack of clinical efficacy may be explained by the low plasma levels of sodium butyrate due to its