Biology Lab Report

BSCI 105 .........................................................

Exercises 9-11, Supplemental: Metabolic Acidosis and the AP Enzyme

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In order to understand the problem outlined in the scenario, it is helpful to place it in the context of real research based on primary literature. This is what you need to do to make a really effective lab report. Although the scenario is fictional, the science behind it is real and should be used in the Introduction, Methods, and Discussion sections of your lab report. In this section, you are provided with simple summaries of the major points of a number of experimental and review papers (so you do not have to read them unless you wan to). You are required to incorporate information from at least two primary sources into your lab report in a sensible way. Do not forget to use in text citations and make a bibliography. The paper you were provided for the Source Summary is the first primary source you should use; for the second (and others) you can refer to this annotated bibliography rather than reading papers yourself.

REMEMBER: Do not plagiarize this annotated bibliography or any other source! You should write your report in YOUR OWN WORDS, and then refer to these or other sources in support of what you are saying. These summaries were written by Dr. Keller, so you need to paraphrase and incorporate any information into your own writing.

ANNOTATED BIBLIOGRAPHY

(1) Bessey, O.A., O.H. Lowry, and M.J. Brock. 1946. A method for the rapid determination of alkaline phosphatase with five cubic millimeters of serum. J. Biol. Chem. 164: 321-329.

This paper was the first publication describing the use of PNP as a substrate for alkaline phosphatase in a spectrophotometric assay.

(2) Fernandez, N.J., and B.A. Kidney. 2007. Alkaline phosphatase: beyond the liver. Vet. Clin. Path. 36: 223-233.

A review of the different types of alkaline phosphatase enzymes found in mammals, including where they are expressed and their use as indicators of various disorders despite a lack of knowledge of specific functions for the enzymes.

(3) Henthorn, P.S., M. Raducha, K.N. Fedde, M.A. Lafferty, and M.P. Whyte. 1992. Different missense mutations at the tissue-nonspecific alkaline phosphatase gene locus in autosomal recessively inherited forms of mild and severe hypophosphatasia. Proc. Natl. Acad. Sci. USA 89: 9924-9928.

This study demonstrates that a variety of mutations in the tissue-nonspecific alkaline phosphatase (TNSALP) can cause phosphate deficiency in humans.

(4) Kovacic, V., L. Roguljic, and V. Kovacic. 2003. Metabolic acidosis of chronically hemodialyzed patients. Am. J. Nephrol. 23: 158-164.

A review of negative effects of metabolic acidosis, including protein breakdown and nitrogen depletion, excessive weight loss, fatigue, bone loss, cardiovascular impairment, exacerbation of chronic renal failure, and growth retardation. The authors make recommendations for treatment of metabolic acidosis in patients with renal failure undergoing hemodialysis, focusing on bicarbonate treatment of blood during dialysis.

(5) Kraut, J. A. 2000. Disturbances of acid-base balance and bone disease in end-stage renal disease. Sem. Dialysis 13: 261-266.

This paper reviews primary literature indicating a causal link between metabolic acidosis and bone disease in patients with chronic renal failure. The authors note that a number of other factors contribute to bone disease as well.

(6) Orimo, H., H.J. Girschick, M. Goseki-Sone, M. Ito, K. Oda, and T. Shimada. 2001. Mutational analysis and functional correlation with phenotype in German patients with childhood-type hypophosphatasia. J. Bone Miner. Res. 16: 2313-2319.

This study finds that different mutations in tissue-nonspecific alkaline phosphatase (TNSALP) can contribute to hypophosphatasia, a disorder characterized by low blood and bone phosphate levels.

(7) Remer, T. 2000. Influence of diet on acid-base balance. Sem. Dialysis 13: 221-226.

A review of the physiological and chemical bases for metabolic acidosis resulting from dietary factors.

(8) Sogabe, N., K. Oda, H. Nakamura, H. Orimo, H. Watanabe, T. Hosoi, and M. Goseki- Sone. 2008. Molecular effects of the tissue-nonspecific alkaline phosphatase gene polymorphism (787T>C) associated with bone mineral density. Biomed. Res. 29: 213-219.

Study demonstrating that differences in bone mineral density among individuals with different alleles of the TNSALP gene are correlated with variation in enzyme activities.

(9) Weiss, M.J., K. Ray, P.S. Henthorn, B. Lamb, T. Kadesch, and H. Harris. 1988. Structure of the human liver/bone/kidney alkaline phosphatase gene. J. Biol. Chem. 263: 12002-12010.

There are at least three genes for alkaline phosphatase in humans, with different expression, regulation and functions.