Aim: to study the processes of lipid peroxidation and the antioxidant defense system in rats with alloxan-induced diabetes against the background of isolated and combined exposure to lead and chromium salts. Materials and methods: an experimental study was conducted on 90 outbred male rats weighing from 230 to 270 g, divided depending on the intoxication caused into 8 subgroups: intact; subgroup “lead”; subgroup “chrome”, subgroup “lead+chrome”; subgroup – alloxan diabetes in intact rats – “control”; subgroup – alloxan diabetes in rats exposed to lead – “lead + alloxan”; subgroup – alloxan diabetes in rats exposed to chromium - “chromium + alloxan”; subgroup - alloxan diabetes in rats that were simultaneously exposed to lead and chromium - “lead + chromium + alloxan”. The rats were slaughtered under ether anesthesia after 30 days of metal priming, as well as on days 3 and 14 after the administration of alloxan. After decapitation, the liver was removed from the animals, washed with cold saline and frozen, then a 10% homogenate was prepared, where the content of diene conjugates, malonic dialdehyde, catalase and superoxide dismutase activity. The concentration of lead and chromium in the blood of rats was determined at the end of a 30-day priming using inductively coupled plasma atomic emission spectrometry. Results: Experimental alloxan diabetes, modeled in terms of the combined action of compounds of lead and chromium, in contrast to alloxan diabetes on isolated background of their action was characterized by a decrease in SOD enzyme activity compared to the level before the introduction of diabetogen. The combined effect of these metals reduces the resistance β-cells of the pancreas to the diabetogenic action of alloxan to a greater extent than their isolated effects. Isolated exposure to lead acetate resulted in increased diene levels conjugates by 13%, the isolated effect of potassium bichromate - by 18%, while the combined effect of lead and chromium - by 50% compared to intact rats. Malon content dialdehyde in the “lead” group and in the “chromium” group increased by 13%, in the “lead + chromium” group – by 68% in relation to intact animals. Increased lipid peroxidation processes in liver cells led to the activation of superoxide dismutase, the activity of which increased by 8% in the lead group, by 21% in the chromium group, and by 45% in the lead + chromium group compared to intact rats. While isolated exposure to lead and chromium had virtually no effect on the enzymatic activity of catalase, the combined influence of metals led to an increase in catalase activity by 13% compared to intact animals. Conclusions: isolated exposure to both lead and chromium activates the processes of lipid peroxidation in the liver of animals to approximately the same extent, does not affect the enzymatic activity of catalase, but the introduction of potassium dichromate activates superoxide dismutase by 12% more than exposure to lead acetate. The combination of these metals activates the processes of lipid peroxidation and the activity of superoxide dismutase to a greater extent than the isolated action of metals, and unlike the isolated action of lead and chromium, the combination of metals increases the activity of catalase.