Abstract
A degenerative cardiomyopathy (DCM) has been observed among mustard oil (MUST) users in China who eat 150 ml/week. Though the condition may be a selenium (Se) deficiency, MUST, rich in erucic acid (22:1), may bear a cardiotoxic or pro-oxidant substrate(s). The purpose of this feeding study was to compare the effects of feeding MUST, high erucic acid rape seed oil (HEAR), low erucic acid rape seed oil (LEAR) and corn oil, with or without Se addenda, on serum cholesterol, triglycerides, thiobarbituric acid reactive substances (TBARS), alpha-tocopherol, platelet aggregation and hepatic glutathione peroxidase (GSHPXase). Heart muscle pathology was evaluated. Eighty male, weanling Wistar rats were divided into four dietary groups and fed AIN76A diet for 8 weeks with one of four oils: 1) MUST, 2) HEAR, 3) LEAR, or CORN oil. Half of each group received 0.43 mg/kg Se supplement. A purified diet was fed for 8 weeks. Neither Se nor oil type affected growth, though serum Se rose with dietary Se addendum (p < 0.01), and hepatic GSHPXase rose for each oil (p < 0.01). Se deprivation led to elevated serum cholesterol, except for the CORN oil group (p < 0.01). Only with LEAR did HDL cholesterol decrease. Serum triglycerides decreased with MUST and LEAR feedings (p < 0.05). In Se deficiency, HEAR led to elevated TBARS (p < 0.01), though not MUST, which contained twice as much alpha-tocopherol. Though supplementary Se protected the HEAR-fed animals from secondary peroxidation as TBARS (p < 0.01), the MUST group was not so protected. Ration Se also spared serum alpha-tocopherol for each diet group except the MUST/Se group (p < 0.05). MUST oil feeding resulted in increased platelet aggregation; MUST and HEAR resulted in increased platelet ATP release compared with CORN oil. Oxidative mechanisms may be involved in the DCM involving both Se limitation and pro-oxidant stress related to the usual intake of MUST. Human studies have been undertaken to test this thesis.
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