Reaction with Fructose Detoxifies Fumonisin B1 while Stimulating Liver-Associated Natural Killer Cell Activity in Rats

Fumonisin B1 (FB1) was reacted with fructose in an attempt to detoxify this mycotoxin. Fischer 344/N rats were initiated with diethylnitrosamine (15 mg/kg body weight) and then fed 69.3 μmol FB1/kg diet or 69.3 μmol FB1 reacted with fructose (FB1−fructose)/kg diet for 4 weeks. In comparison with the rats fed basal diet or FB1−fructose, the FB1-fed rats had significantly increased plasma cholesterol (P \u3c 0.01), plasma alanine aminotransferase activity (P \u3c 0.05), and endogenous hepatic prostaglandin production (P \u3c 0.05). Placental glutathione S-transferase-positive and γ-glutamyl transferase-positive altered hepatic foci occurred only in the FB1-fed rats. Liver-associated natural killer (NK) cell activity was significantly decreased in the FB1-fed rats and increased in the group fed FB1-fructose, as compared with the basal group (P \u3c 0.03). Therefore, modifying FB1 with fructose seems to prevent FB1-induced hepatotoxicity and promotion of hepatocarcinogenesis while stimulating liver-associated NK cell activity in rats

Muscle injuries and repair: The role of prostaglandins and inflammation

Skeletal muscle injuries are a common problem in trauma and orthopaedic surgery. Muscle injuries undergo the healing phases of degeneration, inflammation, regeneration, and fibrosis. Current and experimental therapies to improve muscle regeneration and limit muscle fibrosis include conservative and surgical principles with the adjuvant use of non-steroidal anti-inflammatory drugs (NSAIDs) and growth factor manipulation. NSAIDs appear to have a paradoxical effect on the healing of muscle injuries with early signs of improvement and subsequent late impairment in functional capacity and histology. In vitro and in vivo studies have explored the role of the cyclooxygenases and prostaglandins in the biological processes of healing muscle, including precursor cell activation, myoblast proliferation, myoblast fusion, and muscle protein synthesis. Through use of more specific cyclooxygenase inhibitors, we may be able to better understand the role of inflammation in muscle healing

Inhibited skeletal muscle healing in cyclooxygenase-2 gene-deficient mice: The role of PGE<inf>2</inf> and PGF<inf>2α</inf>

Nonsteroidal anti-inflammatory drugs (NSAIDs) are commonly used to treat skeletal muscle injury. However, studies have shown that NSAIDs may be detrimental to the healing process. Mediated by prostaglandin F 2α (PGF2α) and prostaglandin E2 (PGE2), the cycloxygenase-2 (COX-2) pathway plays an important role in muscle healing. We hypothesize that the COX-2 pathway is important for the fusion of muscle cells and the regeneration of injured muscle. For the in vitro experiments, we isolated myogenic precursor cells from wild-type (Wt) and COX-2 gene-deficient (COX-2-/-) mice and examined the effect of PGE 2 and PGF2α on cell fusion. For the in vivo experiments, we created laceration injury on the tibialis anterior (TA) muscles of Wt and COX-2-/- mice. Five and 14 days after injury, we examined the TA muscles histologically and functionally. We found that the secondary fusion between nascent myotubes and myogenic precursor cells isolated from COX-2-/- mice was severely compromised compared with that of Wt controls but was restored by the addition of PGF2α or, to a lesser extent, PGE2 to the culture. Histological and functional assessments of the TA muscles in COX-2-/- mice revealed decreased regeneration relative to that observed in the Wt mice. The findings reported here demonstrate that the COX-2 pathway plays an important role in muscle healing and that prostaglandins are key mediators of the COX-2 pathway. It suggests that the decision to use NSAIDs to treat muscle injuries warrants critical evaluation because NSAIDs might impair muscle healing by inhibiting the fusion of myogenic precursor cells. Copyright © 2006 the American Physiological Society

Reaction with Fructose Detoxifies Fumonisin B1 while Stimulating Liver-Associated Natural Killer Cell Activity in Rats

Fumonisin B1 (FB1) was reacted with fructose in an attempt to detoxify this mycotoxin. Fischer 344/N rats were initiated with diethylnitrosamine (15 mg/kg body weight) and then fed 69.3 μmol FB1/kg diet or 69.3 μmol FB1 reacted with fructose (FB1−fructose)/kg diet for 4 weeks. In comparison with the rats fed basal diet or FB1−fructose, the FB1-fed rats had significantly increased plasma cholesterol (P P P P Reprinted with permission from Journal of Agricultural and Food Chemistry, 45(3):803-809. doi: 10.1021/jf9607775. Copyright 1997 American Chemical Society.</p