Riboflavin has an impact on wound healing through the general role it plays in hypermetabolic tissues with electron transport and protein/amino acid metabolism as well as its more specific function in tissue repair, and so forth. Specific roles in this process have been established via small animal (rat) research. Research done in the laboratories of Lakshmi et al.11,12 has shown that riboflavin is involved in all of the phases of the wound repair process. In their initial studies,10 rat models were used to examine the relationship between riboflavin deficiency and the healing of both excision and incision wounds. When riboflavin-deficient animals were compared to controls or fasted animals, the period for epithelialization of excision wounds was 4 to 5 d longer in riboflavin-deficient animals compared to weight-matched ad libitum-fed control animals. Riboflavin deficiency as well as food restriction was shown to slow the rate of wound contraction, with riboflavin deficiency having the greater impact of the two treatments. The tensile strength of incision wounds was also reduced 42% in deficient animals when compared to ad libitum-fed controls and 63% compared to weight-matched controls. Total collagen content of incision wounds was also shown to decrease by 25%. Food restriction had similar effects but of lower magnitude. Data suggested that the alteration of collagen content and maturity was responsible for the lower tensile strength in the incision wounds of the riboflavin-deficient rats. This data supported earlier studies by Bosse and Axelrod13 in which riboflavin deficiency was associated with delayed epithelializa-tion of wounds and by Prasad et al.14,15 in which riboflavin-deficient rats were shown, both quantitatively and qualitatively, to have impaired collagen synthesis and cross-linking. The proposed mechanism for this impaired cross-linking of collagen involves riboflavin's role as a carbonyl cofactor for lysyl oxidase activity and the role this enzyme plays in the cross-linking process.16,17
In a subsequent study, Lakshmi et al.11 studied the inflammatory response in riboflavin-deficient rats. In this study, the animals, after having their paws injured, showed a 54% and 52% reduction in critical enzyme activity (nicotinamide adenine dinucleotide phosphate [NADPH] oxidase and superoxide dismutase, respectively) in leukocytes elicited from the peritoneal cavity. Food restriction did not seem to affect this leukocyte enzyme activity. It was concluded that riboflavin deficiency did not enhance inflammation in this model.
The impact that riboflavin has on incisional wound healing has also been studied indirectly by Elbanna et al.18 Thirty-eight surgical patients were monitored for wound healing. The patients were split into two groups with 22 in the control group and 16 in the experimental group. The control subjects were provided with the same meals that other surgical patients received. Experimental subjects were monitored in regards to their diet using a 24 h diet recall system for the 3 d prior to and after surgery. Diets were then modified to optimize nutritional support. Preoperative diet analysis data were used to determine appropriate modifications in nutrition support. Those patients who were found to need preoperative repletion received calories and proteins at levels that were 30 to 50% above maintenance, and minerals, vitamins, and fluids for normal recovery were provided. A wound healing checklist was used to establish recovery. The experimental group had a significantly better score for wound healing than did the control group and the group also had a shorter hospital stay. In the postoperative stage, the dietary intake of riboflavin, as well as protein, iron, calcium, and vitamin A was better than in the control population.
High riboflavin intake is not known to have toxic effects on humans. Some research has shown that when riboflavin and chromium are combined in cell cultures, there is an increase in DNA strand breaks.19
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