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Biochemical response to cadmium. Dose-time effect.

S Khandelwal¹, N Agnihotri, S K Tandon

¹Industrial Toxicology Research Centre, Mahatma-Gandhi Marg, Lucknow, India.

Biological Trace Element Research

|May 1, 1991

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This study reveals that cadmium exposure in rats causes significant changes in liver and kidney function over time. Cadmium accumulation leads to increased metallothionein and enzyme levels, indicating potential organ damage.

Area of Science:

Toxicology
Environmental Health
Biochemistry

Background:

Cadmium (II) is a toxic heavy metal with known adverse health effects.
Understanding the dose- and time-dependent toxicity of cadmium is crucial for risk assessment.

Purpose of the Study:

To investigate the dose- and time-related toxic effects of cadmium (Cd) exposure in rats.
To examine the impact of cadmium on hepatic and renal function, metallothionein induction, and enzyme excretion.

Main Methods:

Rats were administered subcutaneous cadmium chloride (CdCl2.H2O) at 0.5 or 1.0 mg/kg daily for 48 hours, 1, 3, or 6 weeks.
Plasma and urinary enzyme activities (ALP, LDH, GOT, GPT, LAP, gamma-glutamyl transpeptidase), metallothionein levels, and organ mineral content (Zn, Cu) were measured.

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Main Results:

Dose-related increases in plasma enzymes (ALP, LDH, GOT, GPT) were observed at 6 weeks, with an early rise in ALP and LDH at 3 weeks in the higher dose group.
Hepatic and renal metallothionein (MT) induction increased with cadmium dose and duration of exposure.
Urinary enzyme excretion, proteinuria, and aminoaciduria showed a biphasic pattern, with a second phase at 6 weeks correlating with MT induction and organ cadmium levels.

Conclusions:

Cadmium exposure induces significant biochemical alterations in rat liver and kidneys in a dose- and time-dependent manner.
Metallothionein induction serves as a biomarker for cadmium accumulation and subsequent organ toxicity.
Urinary enzyme profiles can indicate cadmium-induced renal damage.