Potassium iodate

Acute Toxicity: other routes

Administrative data

Endpoint:

acute toxicity: other routes

Type of information:

experimental study

Adequacy of study:

key study

Reliability:

2 (reliable with restrictions)

Data source

Reference

Reference Type:

review article or handbook

Title:

Dose doc no. : P255

Author:

RSC Publishing

Year:

2011

Bibliographic source:

Dictionary of Substances and their effects (DOSE); J. Pharmacol. Exp. Ther. 1957, 120, 171.

Materials and methods

Test guideline

Qualifier:

no guideline available

GLP compliance:

not specified

Limit test:

yes

Test material

Test material information

Constituent 1

Reference substance name:

Potassium iodate

EC Number:

231-831-9

EC Name:

Potassium iodate

Cas Number:

7758-05-6

Molecular formula:

HIO3.K

IUPAC Name:

potassium iodate

Test animals

Species:

mouse

Strain:

Swiss

Sex:

male/female

Administration / exposure

Route of administration:

intraperitoneal

Vehicle:

unchanged (no vehicle)

Doses:

140 mg kg-1

Control animals:

not specified

Results and discussion

Effect levels

Sex:

male/female

Dose descriptor:

LD50

Effect level:

140 mg/kg bw

Based on:

test mat.

Remarks on result:

other: other details not available

Applicant's summary and conclusion

Conclusions:

LD50 mouse (i.p) : 140 mg/kg bw

Executive summary:

Abstract

Single-dose, acute toxicity experiments, carried out with white Swiss mice, using potassium and sodium iodates and the corresponding iodides, led to the following conclusions:

Administered in sufficient quantities, the iodates cause intoxication and death. In some instances, death is attributed to renal damage with retention of non-protein nitrogen. Hemolytic effects are evidenced by hemoglobinuria and, histologically, by hemoglobin casts and hemosiderin deposits in the kidneys.

Fatty visceral changes, non-specific in nature, appear within 24 hours after ingestion of iodates or iodides. Similar changes occur in fasted animals.

Oral administration of iodates, at levels of 140 to 500 mgm./kgm., often increase the pH of the gastric contents. This is frequently accompanie by degenerative changes in the parietal cells. The damage is transient, as evidenced by restoration to normal in histological appearance of the gastric mucosa and in the pH values after 24 hours. Intraperitoneal and intravenous injections of iodates have little effect on the gastric pH.

The toxicity of potassium iodate varies greatly with the route of administration; the oral LD₅₀for mice fasted on sawdust overnight is six times that of the intraperitoneal LD₅₀. Potassium iodate and sodium iodate have nearly identical oral toxicities and similar intraperitoneal toxicities; the oral toxicity of the potassium compound is nearly the same for heavy and light mice and for both sexes, and is not increased in weanling animals.

Similarly, the relative toxicities of iodates and iodides depend on route of administration and on previous treatment of the mice.