Bovine lactoferrin ameliorates ferric nitrilotriacetate-induced renal oxidative damage in rats

Our plain-English summary of Bovine lactoferrin ameliorates ferric nitrilotriacetate-induced renal oxidative damage in rats, by Y. Okazaki, I. Kono, T. Kuriki, et al (Journal of Clinical Biochemistry and Nutrition, 2012).

The study

• Authors: Y. Okazaki, I. Kono, T. Kuriki, S. Funahashi, S. Fushimi, M. Iqbal, S. Okada, S. Toyokuni
• Journal: Journal of Clinical Biochemistry and Nutrition
• Published: 2012;51(2):84-90
• Cited by: 22 articles, as counted by NIH iCite
• Read it: PubMed · Publisher · Free full text

Abstract

Milk provides a well-balanced source of amino acids and other ingredients. One of the functional ingredients in milk is lactoferrin (LF). LF presents a wide variety of bioactivities and functions as a radical scavenger in models using iron-ascorbate complexes and asbestos. Human clinical trials of oral LF administration for the prevention of colon polyps have been successful and demonstrated that dietary compounds exhibit direct interactions. However, antioxidative properties of LF in distant organs require further investigation. To study the antioxidant property of LF, we employed bovine lactoferrin (bLF) using the rat model of ferric nitrilotriacetate (Fe-NTA)-induced renal tubular oxidative injury. We fed rats with bLF (0.05%, w/w) in basal chow for 4 weeks and sacrificed them after Fe-NTA treatment. After intraperitoneal administration of 9.0 mg iron/kg Fe-NTA for 4 and 24 h, bLF pretreatment suppressed elevation of serum creatinine and blood urea nitrogen levels. In addition, we observed protective effects against renal oxidative tubular damage and maintenance of antioxidant enzyme activities in the bLF-pretreated group. We thus demonstrated the antioxidative effect of bLF against Fe-NTA-induced renal oxidative injury. These results suggest that LF intake is useful for the prevention of renal tubular oxidative damage mediated by iron.

In plain English

This was an animal experiment in male Wistar rats. It did not study asbestos, which appears only in background describing other research on lactoferrin, a milk protein. The authors fed rats a diet containing 0.05% bovine lactoferrin for 4 weeks. They then injected ferric nitrilotriacetate (Fe-NTA), an iron compound that damages the kidney, into the abdomen at 9.0 mg iron per kg body weight. Thirty-two rats were divided into untreated, lactoferrin-alone, Fe-NTA-alone and lactoferrin-plus-Fe-NTA groups. Fe-NTA raised blood creatinine and urea nitrogen, markers of kidney failure, at 4 and 24 hours, and lactoferrin pretreatment suppressed these rises. Lactoferrin also prevented the fall in kidney glutathione and in two antioxidant enzyme activities, and fewer kidney tubules showed oxidatively damaged proteins. In 18 other rats, lactoferrin in the diet did not slow growth. The authors concluded that lactoferrin protected against iron-induced kidney tubule injury in rats. They noted that they did not measure non-transferrin-bound iron in the blood or the rats' own lactoferrin in the kidney.

We wrote this plain-English summary from the full article with the help of AI, and a second AI model checked each sentence against the article. It is not the authors' wording; the abstract and the article are their own account.

What the study did and found

• Design: Animal experiment: rats randomly divided into groups, with and without dietary bovine lactoferrin and with and without Fe-NTA injection
• Who was studied: Male Wistar rats, 4 weeks old at purchase. 32 rats were used in the antioxidant experiment and 18 rats in a separate growth experiment. Experiments were approved by Okayama University in Japan.
• Exposure: Bovine lactoferrin in powdered chow (0.05% w/w) for 4 weeks, followed by a single intraperitoneal injection of ferric nitrilotriacetate (Fe-NTA) at 9.0 mg iron/kg body weight. No asbestos exposure was studied.
• Main results:
  • Fe-NTA raised serum creatinine and blood urea nitrogen at 4 and 24 hours. Lactoferrin pretreatment suppressed these rises at both time points.
  • Kidney reduced glutathione fell 4 hours after Fe-NTA in rats without lactoferrin. This change was significantly suppressed by lactoferrin pretreatment.
  • In rats given lactoferrin alone, kidney glutathione rose slightly, but not statistically significantly (p = 0.25).
  • Four hours after Fe-NTA, glutathione peroxidase and glutathione reductase activities in the kidney decreased. Lactoferrin pretreatment prevented this.
  • In Fe-NTA-treated rats, the number of kidney tubules stained for HNE-modified proteins (a sign of oxidative damage) was significantly lower in the lactoferrin-treated group.
  • At 24 hours, Fe-NTA caused massive destruction of proximal tubules. With lactoferrin pretreatment, this damage was confined to localized areas.
  • Lactoferrin feeding at 1, 0.5, 0.1, 0.05 and 0.01% did not slow growth.
  • Transferrin saturation was 24.7 plus or minus 2.54% in untreated controls and 22.6 plus or minus 0.69% in rats given lactoferrin alone (n = 4; p = 0.44).
• The authors' conclusion: The authors concluded that bovine lactoferrin had protective effects against iron-induced renal tubular injury in rats. They also stated that further study is needed to identify human conditions where such prevention would be useful.
• Limitations the authors state:
  • The authors did not measure non-transferrin-bound iron in the blood.
  • The authors did not determine the rats' own (endogenous) lactoferrin in the kidney.
  • The proposed mechanisms of protection were not tested and require further investigation.

Topics

Medical terms in this study, explained in our Lexicon: Clinical Trial.

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