Anaerobic respiring bacteria and methanogens play an essential role in the biological cycles of carbon, nitrogen and sulfur. In general, they convert oxidized forms of the elements to a more reduced state. The lithotrophic procaryotes metabolize the reduced forms of nitrogen and sulfur to a more oxidized state in order to produce energy. The methanotrophic bacteria , which uniquely posses the enzyme methane monooxygenase, can oxidize methane as a source of energy. Among all these groups of procaryotes there is a minicycle of the elements in a model ecosystem.
NADH and NADPH are redox cofactors, primarily involved in catabolic and anabolic metabolic processes respectively. In addition, NADPH plays an important role in cellular antioxidant defence. In live cells and tissues, the intensity of their spectrally-identical autofluorescence, termed NAD(P)H, can be used to probe the mitochondrial redox state, while their distinct enzyme-binding characteristics can be used to separate their relative contributions to the total NAD(P)H intensity using fluorescence lifetime imaging microscopy (FLIM). These protocols allow differences in metabolism to be detected between cell types and altered physiological and pathological states.
Hartnup disorder is an autosomal recessive impairment of neutral amino acid transport affecting the kidney tubules and small intestine. The disorder results from defects in the specific transport system responsible for neutral amino acid transport across the brush-border membrane of renal and intestinal epithelium. Deficiencies in the solute carrier family 6 (neurotransmitter transporter), member 19 gene (symbol SLC6A19) are associated with Hartnup disorder. The encoded protein is also referred to as the system B(0) neutral amino acid transporter 1 [B(0)AT1] protein. The characteristic diagnostic feature of Hartnup disorder is a dramatic neutral hyperaminoaciduria. Additionally, individuals excrete indolic compounds that originate from the bacterial degradation of unabsorbed tryptophan. The reduced intestinal absorption and increased renal loss of tryptophan lead to a reduced availability of tryptophan for nicotinamide adenine dinucleotide (NAD + and NADP + ) biosynthesis. As a consequence affected individuals frequently exhibit pellegra-like rashes