Glutathione (GSH), the most abundant intracellular low molecular weight thiol, has diverse physiological roles, and altered GSH status has been implicated in a number of chronic, acute, and age-related diseases, as well as the aging process itself. Its function as an antioxidant and determinant of cellular redox potential is crucial both for protection from reactive oxygen species as well as a signaling molecule involved in cellular proliferation, cell cycle regulation, and apoptosis. It is also an important thiol buffer, maintaining sulfhydryl groups in their reduced form, an additional mechanism for cellular signaling. Glutathione has also emerged a key modulator of xenobiotic toxicity, most notably the persistent organic pollutants which are associated with many diseases of impaired metabolic activity, including diabetes, obesity, and cardiovascular disease. γ-glutamyl transpeptidase (GGT), an enzyme critical to the catabolism of GSH and its conjugates, appears to be an important biomarker for xenobiotic exposure, and for increased GSH demand. We review the physiological functions of glutathione, the limiting factors for its synthesis, as well as its clinical relevance, with particular emphasis on detoxification of environmental pollutants. We also review therapeutic approaches for enhancing GSH status.

The concept of diet-induced ‘acidosis’ as a cause of disease has been a subject of interest for more than a century. The present article reviews the history of our evolving understanding of physiological pH, the physiological support for the concept of ‘acidosis’, the causes of acidosis, how it is recognised, its short-term effects as well as the long-term clinical relevance of preventative measures, and the research support for normalisation of pH. Further, we suggest differentiation of the terms ‘acidosis’ and ‘acidaemia’ as a way to resolve the conflation of these topics which has led to confusion and controversy. The available research makes a compelling case that diet-induced acidosis, not diet-induced acidaemia, is a real phenomenon, and has a significant, clinical, long-term pathophysiological effect that should be recognised and potentially counterbalanced by dietary means.

The comparative absorption of zinc after oral administration of three different complexed forms was studied in 15 healthy human volunteers in a double-blind four-period crossover trial. The individuals were randomly divided into four groups. Each group rotated for four week periods through a random sequence of oral supplementation including: zinc picolinate, zinc citrate, and zinc gluconate (equivalent to 50 mg elemental zinc per day) and placebo. Zinc was measured in hair, urine, erythrocyte and serum before and after each period. At the end of four weeks hair, urine and erythrocyte zinc levels rose significantly (p less than 0.005, p less than 0.001, and p less than 0.001) during zinc picolinate administration. There was no significant change in any of these parameters from zinc gluconate, zinc citrate or placebo administration. There was a small, insignificant rise in serum zinc during zinc picolinate, zinc citrate and placebo supplementation. The results of this study suggest that zinc absorption in humans can be improved by complexing zinc with picolinic acid.

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