Combined selenium and vitamin C deficiency causes cell death in guinea pig skeletal muscle

Abstract

Combined antioxidant deficiencies of selenium and vitamin E or vitamin E and vitamin C in guinea pigs result in clinical illness. We hypothesized that combined selenium and vitamin C deficiency would have clinical consequences because in vitro interactions of these antioxidant nutrients have been reported. Since guinea pigs are dependent on dietary vitamin C, weanling male guinea pigs were fed selenium-deficient or control diet for 15 weeks prior to imposing vitamin C deficiency. Four dietary groups were formed and studied 3 weeks later: controls, vitamin C deficient, selenium deficient, and doubly deficient. Deficiencies were confirmed by determinations of glutathione peroxidase activity and vitamin C concentration in liver and skeletal muscle. Plasma creatine phosphokinase (CPK) activity and liver, kidney, heart, and quadriceps histopathology were determined. Doubly deficient animals had moderately severe skeletal muscle cell death as judged by histopathology and plasma CPK activity of 6630 ± 4400 IU/L (control 70 ± 5; vitamin C deficient 95 ± 110; selenium deficient 280 ± 250). Liver, kidney, and heart histology was normal in all groups. Muscle α-tocopherol levels were not depressed in the doubly deficient group but muscle F 2 isoprostane concentrations were elevated in them and correlated with markers of cell death. We conclude that combining selenium and vitamin C deficiencies in the guinea pig causes cell death in skeletal muscle that is more severe than the injury caused by selenium deficiency. The elevation of muscle F 2 isoprostanes is compatible with the cell death being caused by oxidative stress.

Chronic vitamin E deficiency impairs cognitive function in adult zebrafish via dysregulation of brain lipids and energy metabolism

“…These results contrast with our previous findings where fish had combined VitE and vitamin C deficiencies that caused significant myopathy in the E− adults and impaired startle responses [22]. These latter findings were expected because compound antioxidant-nutrient deficiencies frequently lead to significantly more severe pathophysiological (myopathic) consequences than do isolated deficiencies [36,37]. When E− fish were fed a VitE-deficient diet with excess vitamin C (3500 mg/kg) and soybean lecithin (which has only 20% PC), we found that the E− swam slower and with multiple taps became speedier [21].…”

Chronic vitamin E deficiency promotes vitamin C deficiency in zebrafish leading to degenerative myopathy and impaired swimming behavior

“…In humans, the rate of disappearance of vitamin E in response to oxidative stress is dependent on vitamin C status (Bruno et al, 2005). In guinea pigs, vitamin C deficiency alone does not cause significant muscle damage, but does exacerbate vitamin E or selenium deficiencies and the resultant myopathies (Hill et al, 2003; Hill et al, 2009). Like humans and guinea pigs, zebrafish require both vitamins in the diet.…”

Potential Role of Tocotrienols on Non-Communicable Diseases: A Review of Current Evidence

“…Studies have also shown that muscle health is dependent on an adequate supply of dietary vitamin E which includes T3 [180]. A diet deficient in vitamin E causes profuse myocyte necrosis and ultimately leads to lethal muscular dystrophy, as demonstrated in various animal model studies [181][182][183][184].…”