Fermented camel milk prevents carbon tetrachloride induced acute injury in kidney of mice.

Fermented milk is known to possess potent antioxidant activity. The present study was undertaken to assess the preventive effect of fermented camel milk (FCM) prepared using lactococcus lactis subsp. cremoris against CCl4 induced kidney damage in mice. Nephrotoxicity was induced in mice by a single dose of CCl4 (10 ml/kg 0·3% olive oil, ip). Female mice were pretreated daily with FCM for 15 d. Renal damage was associated with an increase in oxidative stress parameters (lipid peroxidation, protein carbonyl and changes in antioxidant enzyme activities and non-enzymatic antioxidant) and nephropathology markers.The renal injury induced by CCl4 was confirmed by the histological study of the CCl4-intoxicated mice. Pretreatment with FCM significantly prevented renal dysfunction by reducing oxidative stress, while mice recovered normal kidney histology. Moreover, FCM prevented toxicity biomarker changes by reducing creatinine, urea, uric acid, lactate dehydrogenase (LDH) and electrolytes levels in plasma. These data indicate that FCM is efficient in inhibiting oxidative stress induced by CCl4, and suggests that the administration of this milk may be helpful in the prevention of kidney damage.

Cardiopreventive effects of camel milk against carbon tetrachloride induced oxidative stress, biochemical and histological alterations in mice.

The present study was designed to examine the preventive effects of camel milk (CM) against the toxic effects of acute exposure to carbon tetrachloride (CCl4) on the heart tissue of mice. Administration of a single dose of CCl4 caused cardio toxicity as monitored by an increase in lipid peroxidation (thiobarbituric acid reactive substances), protein carbonyl level and antioxidant markers (superoxide dismutase, catalase, glutathione peroxidase, glutathione and vitamin C) in the heart tissue. Moreover, CCl4 caused a distinguished rise of plasma aspartate aminotransferase, lactate dehydrogenase, troponin I, and creatine kinase activities. Furthermore, CM ameliorated biochemical and histological parameters as compared to CCl4-treated group. Overall, this study indicates that CM is efficient in inhibiting oxidative stress induced by CCl4 and suggests that the administration of this milk may be helpful in the prevention of cardio-toxicity complications.

Beneficial effects of fermented camel milk by lactococcus lactis subsp cremoris on cardiotoxicity induced by carbon tetrachloride in mice.

Carbon tetrachloride (CCl4) is a xenobiotic present in the environment, can cause harmful effects on human health. In the present study, we attempted to elucidate the cardiopreventive potential of the fermented camel milk by lactococcus lactis subsp cremoris (FCM-LLC) against the toxic effects of acute exposure to CCl4 on heart tissue of mice. Twenty-eight mice's were divided into four groups of seven each: group (C) served as control; group (FCM-LLC) received only 100mgL of FCM-LLC/kg body weight daily for 15days; group (CCl4) was administered by a single dose of CCl4 (10mL/kg in 0.3% olive oil, i.p) at day 14 and group (FCM-LLC+CCl4) pretreated with FCM-LLC and received a single dose of CCl4 on day 14. The exposure to a single dose of CCl4 caused cardiotoxicity expressed by an increase in lipid peroxidation (TBARS), protein carbonyls (PC) levels and in antioxidant markers (superoxide dismutase (SOD), catalase (CAT), gluthathione peroxidase (GPx), glutathione (GSH) and Vitamin C levels) in the CCl4-treated group when compared with the untreated group. Furthermore, treatment with CCl4 significantly elevated the cardiac toxicity markers while increasing of alanine aminotransferase (ALT), lactate dehydrogenase (LDH), creatine kinase (CK), creatine kinase MB (CKMB) and Troponin I activities. The pre-treatment of experimental mice's with FCM-LLC has allowed an improvement through lowering oxidative stress and attenuating cardiac toxicity. These modifications were further evident through histopathological aspects of the heart. Overall, the present data provide evidence of the beneficial effects of fermented camel milk by lactococcus lactis subsp creemoris clearly revealed through the reduction of the CCl4 induced heart oxidative damages.

Fermented camel milk by Lactococcus lactis subsp. cremoris attenuates erythrocytes oxidative stress-induced hematological and immunological damage in CCl4-intoxicated mice.

Fermented camel by Lactococcus lactis subsp. cremoris has been recently discovered to protect against the toxic effect of carbon tetrachloride (CCl4), but its beneficial effects in the presence of oxidative stress in the erythrocytes have not been established. In the present study, 28 mice were randomly divided into four groups: control group; CCl4 group: intoxicated by a single intraperitoneal injection (ip) of CCl4; group FCM-LLC + CCl4: pretreated with FCM-LLC daily during 14 days, and received a single dose of CCl4. FCM-LLC group received FCM-LLC alone. The occurrence of oxidative stress in erythrocytes was evidenced by an increase in lipid peroxidation, protein carbonyl, and changes in antioxidant enzyme activities and non-enzymatic antioxidant. The oxidative injury induced by CCl4 in the erythrocytes was confirmed by modifications in hematological parameters and decreases in protein, albumin, and globulin content in the serum of intoxicated mice. Therefore, CCl4 caused a significant decrease in immunotoxic indices, including immunoglobulin G (IgG), immunoglobulin M (Ig M), and immunoglobulin A (IgA) levels, and an increase of inflammatory markers such as C-reactive protein (CRP) level. Meanwhile, FCM-LLC effectively restored the parameters cited above to near-normal values. It can be suggested that fermented camel milk could regulate deviant physiological effects induced by CCl4 which is due to its powerful antioxidant and immunomodulatory and anti-inflammatory capacity.