Muscle degeneration in chicks caused bySenna occidentalisseeds

Abstract

Acute intoxication with Senna occidentalis seeds was studied in chicks. Seven-day-old chicks were fed ground dried seeds of this plant mixed with regular chicken ration at a concentration of 4% by weight for 15 days. Feed intake and body weight were markedly affected and a high level of lethality was observed. Necropsy examination of chicks from the experimental group revealed paleness and atrophy of thoracic muscles. Degenerative and necrotic fibres were observed in skeletal muscle by histological examination. Muscle histochemistry showed accumulation of lipids and numerous acid phosphatase-positive muscle fibres. Electron microscopy revealed atrophic muscle fibres, lipid storage, dilatation of the sarcoplasmic reticulum and abnormal mitochondria.

Effect of Senna occidentalis Seeds on Immunity in Broiler Chickens

“…It is well known that damage in the immune system generally can be produced with lower doses of xenobiotics than those which induce overt toxic effects in other systems (Sjoblad, 1988). Previous studies, conducted in this laboratory, revealed that prolonged administration of So seeds in concentrations of 1% in the diet can cause lesions in cardiac and skeletal muscle in broiler chicks (Haraguchi et al., 1998a,b). In contrast to these other results, at the concentrations employed here (0.25%, 0.50% and 0.75% So seeds) did not induce lesions characteristic of So toxicosis.…”

“…Many studies revealed that So exposure, regardless of the animal species, promotes anorexia and a remarkable loss of body weight (Torres et al., 1971; Barth et al., 1994; Haraguchi et al., 1998a,b; Tasaka et al., 2000). Moreover, it is well known that nutritional deficiencies such as lack of protein, energy, copper, zinc, folic acid, vitamins and other compounds can impair the immune system, and, increase susceptibility to infectious diseases (Scrimshaw and SanGiovanni, 1997).…”

“…Electron microscopy studies of affected muscle fibres revealed the presence of mitochondrial damage promoted by So , denoting that this myopathy is secondary to impairment of mitochondria function (Graziano et al., 1983; Calore et al., 1997, 1999, 2000; Haraguchi et al., 1998a; Tasaka et al., 2000); however, the exact mechanism of action of So toxin on mitochondrial metabolism is still unknown. On the other hand, a study conducted by Lewis and Shibamoto (1989) with Senna obtusifolia showed that this toxic plant can cause impairment of mitochondrial metabolism inhibiting NADH oxidation and electron transport in mitochondria, resulting in uncoupling of oxidative phosphorylation.…”

“…The main toxic principles of So seed have been identified as dianthrone (Haraguchi et al., 1996), an anthraquinone‐derived compound in So seeds that promotes the characteristic mitochondrial myopathy produced by this plant (Graziano et al., 1983; Calore et al., 1997, 1999, 2000; Haraguchi et al., 1998a,b; Tasaka et al., 2000). Furthermore, So toxicity in chickens has been proposed to impair mitochondrial function, resulting in swelling, loss of mitochondrial matrix, fragmented mitochondrial cristae and glycogen depletion (O'Hara and Pierce, 1974; Calore et al., 1997).…”

Toxicity of Senna occidentalis seeds in laying hens and its effects on egg production

“…The main toxic component of S. occidentalis seed was identified by our group as dianthrone (Haraguchi et al, 1996), an anthraquinone-derived compound that is found in the external and internal tegument (ET/IT) of the seeds (Haraguchi et al, 1998b). It was shown that this substance can cause the characteristic mitochondrial myopathy with an impairment of mitochondrial function, including swelling, loss of mitochondrial matrix, fragmented mitochondrial cristae and glycogen depletion (Calore et al, 1997).…”