The Vitamin E analog Trolox reduces copper toxicity in the annelid Lumbriculus variegatus but is also toxic on its own.

The ability of the water-soluble Vitamin E analog, Trolox, to prevent the toxic effects of copper exposure on the behavior and neuronal physiology of the freshwater oligochaete Lumbriculus variegatus was examined. Trolox produced a concentration-dependent increase in the 24 h LC(50) for copper exposure, with 100 microM Trolox elevating the LC(50) by almost seven-fold (from 0.36 to 2.43 microM). Copper exposure (0.2 microM) for 24h produced a reduction in the conduction velocity of the medial and lateral giant nerve fibers, which was prevented by 100 microM Trolox. Copper exposure (0.2 microM) for 24h also reduced the effectiveness of substrate vibration in eliciting giant nerve fiber spikes. Trolox prevented this reduction in sensory responsiveness. Trolox (100 microM) partially reversed the copper-induced (0.4 microM) decrease in touch-evoked helical swimming behavior, but had no effect on the copper-induced decrement in touch-evoked body reversal. Copper exposure (0.2 microM) for 24 h reduced the amount of spontaneous locomotion (crawling); however, Trolox did not reverse this effect. However, Trolox exposure alone produced a decrease in the distance crawled that was similar in magnitude to copper exposure. In normal worms, rapid spiking activity of the medial giant nerve fiber produces facilitation in the amplitude of the resulting muscle potentials produced by the longitudinal body wall muscles. Copper exposure had no effect on the amount of muscle potential facilitation, but Trolox exposure (100 microM) produced a significant decrease in facilitation. The results of this study indicate that many of the toxic effects of copper exposure on Lumbriculus are prevented or reduced by the antioxidant Trolox. However, the results of this study also indicate that Trolox has toxic effects on behavior and neuronal physiology. The results presented here document one of the few published reports of the detrimental effects of Vitamin E or its analogs on nervous system function or behavior.