ABSTRACT
The current was conducted to evaluate the ameliorating effect of Chlorella vulgaris (CV) extract against sodium nitrite-induced hepatotoxicity in rats. Forty-five rats were allocated randomly into 5 groups (n = 9). Group I (GI), control group: orally gavaged with normal saline daily. Group II (GII): orally gavaged with CV extract (70 mg/kg BW) for 3 months. Group III (GIII): orally gavaged with sodium nitrite (80 mg/kg BW) for 3 months. Group IV (GIV): received sodium nitrite as GIII and CV extract as GII simultaneously for 3 months. Group V (GV): received CV extract as GII and then, sodium nitrite as in GIII from the end of first month until the end of the experiment. Sodium nitrite significantly increased the activities of serum alanine aminotransferase, aspartate aminotransferase, and serum concentrations of tumor interleukin 1-ß and necrosis factor α. In addition, it increased concentrations of malondialdehyde and nitric oxide and expression level of caspase-3 in the hepatic tissue. However, it decreased activities of hepatic glutathione peroxidase, catalase, and superoxide dismutase and induced degenerative and necrotic changes in hepatic tissues. In contrast, CV extract administration modulated sodium nitrite-induced inflammation, oxidative stress, and alteration in hepatic tissue function and architecture. This study indicated that CV extract modulated sodium nitrite-induced hepatic toxicity through decreasing oxidative stress and inflammation and enhancing antioxidant enzyme activities in hepatic tissue of rats.
Subject(s)
Chemical and Drug Induced Liver Injury , Chlorella vulgaris , Animals , Antioxidants , Chlorella vulgaris/metabolism , Glutathione/metabolism , Liver/metabolism , Oxidative Stress , Rats , Sodium Nitrite/toxicity , Superoxide Dismutase/metabolismABSTRACT
The current study aimed to investigate the protective potential of Chlorella Vulgaris (CV) extract against the reproductive dysfunction induced by sodium nitrite toxicity. Forty-five male Wistar albino rats were assigned into five groups (n = 9). Control group received normal saline orally for 3 months, CV-treated: administered CV extract (70 mg/kg.BW) orally for 3 months, sodium nitrite-treated: received sodium nitrite (80 mg/kg.BW) orally for 3 months, co-treated: simultaneously received CV along with sodium nitrite treatment, orally, daily for 3 months, and CV-pre-treated: pre-treated with CV extract for 4 weeks followed by simultaneous treatment with sodium nitrite and CV extract for additional 8 weeks. Treatment with sodium nitrite significantly decreased serum testosterone and follicle-stimulating hormone concentrations, sperm count, motility, and viability. Besides, it decreased testicular superoxide dismutase and glutathione peroxidase activities while increased malondialdehyde concentration. This effect of sodium nitrite was associated with degenerative, necrotic, vascular, and inflammatory changes in testicular tissues. Treatment of sodium nitrite-intoxicated rats with CV in co-treated and pre-treated groups significantly prevented sodium nitrite-induced alterations of sperm parameters, hormonal concentrations, testicular oxidative-antioxidant status, and histological architecture. This study indicates that CV extract ameliorates the reproductive dysfunction induced by sodium nitrite toxicity via improving reproductive hormonal levels and testicular antioxidant activities.
