Basic copper zinc nitrate

Direct observations: clinical cases, poisoning incidents and other

Administrative data

Endpoint:

direct observations: clinical cases, poisoning incidents and other

Type of information:

other: case report

Adequacy of study:

supporting study

Study period:

n.a.

Reliability:

2 (reliable with restrictions)

Rationale for reliability incl. deficiencies:

other: case report

Data waiving:

other justification

Justification for data waiving:

other:

Data source

Reference

Reference Type:

publication

Title:

Unnamed

Year:

1998

Report date:

1998

Materials and methods

Study type:

clinical case study

Endpoint addressed:

acute toxicity: oral

Test guideline

Qualifier:

no guideline available

GLP compliance:

no

Test material

Test material information

Constituent 1

Reference substance name:

7758-99-8

Cas Number:

7758-99-8

IUPAC Name:

7758-99-8

Constituent 2

Reference substance name:

copper sulfate pentahydrate

IUPAC Name:

copper sulfate pentahydrate

Details on test material:

ingestination of 8 g copper sulfate pentahydrate in suicida attempt

Method

Subjects:

n.a. emergency in hospital

Route of exposure:

oral

Reason of exposure:

other: suicida attempt

Exposure assessment:

estimated

Results and discussion

Clinical signs:

He was lethargic and vomiting spontaneously. Blue staining of the oral mucosaand vomitus on his clothes were
noticed. The temperature was 36.2°C, the pulse rate was 92, the respirations were 30, and the blood pressure was 160/64
mmHg.Noneurological focal sign was present on examinations. The laboratory data revealed hemoconcentration with
18.7 g/dl of hemoglobin and 55% of hematocrit. Although indirect bilirubin was 1.4 mg/dl, other renal and liver function
tests remained in the normal limit.

Applicant's summary and conclusion

Conclusions:

Ingested copper induces mucous irritation, nausea, vomiting and diarrhea.
Ionizied copper is rapidly absorbed from the stomach and the intestine, and the serum copper level increases rapidly. The element
is bound to alabumin and ceruloplasmin, and is taken up by the liver, kidney, lungs and red blood cells. Hemeolytic anemia and
renal tubular neucrosis may followed by 36-48 hours after exposure. The primary route of excretion is thourgh bile and feces.

The toxicity of copper at a cellular level is probably related to the sulfhyryl moieties of glucose-6-phosphtate dehydrogenase
and glutathione, thereby reducing their free radical scavenging activities. Copper
induces hemolysis through oxidation of hemoglobin sulfhydryl groups. Copper also inhibits Na+/K(+)-ATPase and increases
the permeability of cell membrane. Since copper is known to damage human skeletal muscle cells, copper intoxication
could cause rhabdomyolysis. Althougha case of copper-induced acute rhabdomyolysis in Wilson's disease was
reported , rhabdomyolysis in acute copper intoxication has been rarely reported . This might be because myoglobinuria
might be overlooked by the coexistence of hemoglobinuria secondary to hemolytic anemia.