Alterations in Sulfolipid Metabolism in Malathion-Stressed Rats

The effects of malathion stress on, inorganic sulfur metabolism in female rats were investigated by extracting macromolecules containing ester sulfate from cellular lipoprotein. Sulfolipid, mucopoly saccharide, nucleotide, and sulfate transfer fraction were extracted from the lipoprotein prepared from five to seven pooled livers from rats fed diets containing 0.42, 0.10, and 0.0002 percent sulfate. Six groups of rats (two groups per diet) were fed the diets for 21 days. Rats were given either malathion in corn oil or only corn oil by stomach tube every 24 hours for three days and were killed on day 21. Lipoprotein was isolated from liver by exhaustive salt extraction. Determination of the specific activities of the macromolecules from lipoprotein by liquid scintillation counting revealed a statistically significant increase in ³⁵SO₄⁼ incorporation into sulfolipid of malathion-stressed rats as compared with controls fed the diet containing 0.10 percent sulfate. In general, malathion stress caused increases in specific activities of liver lipoprotein macromolecules. These increases were generally intensified by decreasing the level of dietary sulfate.

An investigation was initiated in order to identify the cellular component and the mechanism causing the increased ³⁵SO4⁼ incorporation into sulfolipid observed in malathion-stressed rats. Total galactose, sulfate, and ³⁵S activity were determined in liver lipoprotein sulfolipid extracted from nuclei, mitochondria, and the residue from groups of 16 and 20 pooled livers from malathion-stressed rats and controls, respectively. These rats were fed the diet containing 0.10 percent sulfate. Data indicated that nuclear sulfolipid was the component of lipoprotein most active in ³⁵SO₄⁼ incorporation and probably was responsible for the increased ³⁵S activity previously observed in cellular lipoprotein sulfolipid. The galactose sulfate molar ratio in cellular lipoprotein sulfolipid from the cell particulates indicated that sulfate was being mobilized from sulfolipid.

Arylsulfatase activity was estimated in groups of three pooled livers from malathion-stressed rats and controls (five groups each) fed the diet containing 0. 10 percent sulfate. A statistically significant increase in arylsulfatase activity per mg of nitrogen was found in liver homogenates of malathion-stressed rats as compared with controls. This finding provided further evidence for the mobilization of sulfate from sulfolipid from malathion-stressed rats.