This study compared taurine, aminomethanesulfonic acid, homotaurine and hypotaurine for the ability to modify indices of oxidative stress and membrane damage associated with type 2 diabetes. In the study, male Goto-Kakizaki and Wistar-Kyoto rats were allowed free access to a high fat and normal diet, respectively, for 9 weeks. At the end of week 8, half of the animals in each group received a daily intraperitoneal dose of a sulfur compound (0.612 M/kg) for 5 days and, 24 hr after the last treatment, blood samples were withdrawn by cardiac puncture to obtain plasma and erythrocyte fractions for biochemical analyses. Relative to control values, taurine and its congeners reduced membrane damage, the formation of intracellular malondialdehyde and oxidized glutathione, and the decreases in reduced glutathione and antioxidative enzyme activities in diabetic erythrocytes. Except for a few isolated instances, all test compounds were equiprotective.

Taurine (TAU) and compounds representing a TAU analog (hypotaurine = HYTAU) or homolog (aminomethanesulfonic acid = AMSA, homotaurine = HMTAU) were tested for their counteracting effects against alterations in erythrocyte (RBC) morphology, membrane fluidity and cytoskeletal spectrin distribution due to diabetes, alcoholism and diabetes-alcoholism in male Goto-Kakizaki rats (made diabetic with a high fat diet and alcoholic upon feeding on a flavored alcohol solution) and Wistar-Kyoto rats (serving as controls). Both diabetes and alcoholism changed the RBC discoidal biconcave shape to a spiculated one, lowered membrane fluidity, and caused spectrin to become marginalized. While AMSA and HYTAU returned the RBC shape to normal, HMTAU made it only discoidal, and TAU was without effect. All test compounds, but TAU, maintained the membrane fluidity normal; and HYTAU and AMSA, but not TAU or HMTAU, kept spectrin uniformly distributed. The noted effects were correlated with compound structure and RBC values for malondialdehyde and cholesterol/phospholipid ratio.

A high performance liquid chromatographic (HPLC) method, with fluorometric detection, was developed for studying the oral absorption and ensuing plasma pharmacokinetics of (þ)-catechin and (2)-epicatechin in a small animal model. A plasma sample was first incubated with buffered b-glucuronidase plus sulfatase to release the catechins from their conjugated forms, and next deproteinized with methanol-perchloric acid (3 þ 2) mixture containing an internal standard ((þ)-catechin for the assay of (2)-epicatechin and the latter for the assay of the former). Analyses were carried out on a Microsorb-MV C18 column, with methanol-waterformic acid (15 : 84 : 1) flowing at 1 mL/min, and a fluorometric detector set at an excitation wavelength of 280 nm and an emission wavelength of 310 nm. (þ)-Catechin and (2)-epicatechin eluted at 6.7 min and 13.8 min, respectively. Detector responses were linearly related to concentrations of catechin compound in the range 5 -160 nM (r 2 !0.993). The limits of detection were 0.75 nM for (þ)-catechin and 1.5 nM for (2)-epicatechin. Accuracy and precision were evaluated at three concentrations of each catechin compound. Recoveries of (þ)-catechin and (2)-epicatechin from spiked rat plasma ranged from 95.0 to 101.8% and from 98.7 to 102.5%, respectively. The RSD values for interday variability were in the range 1.27-4.07% for (þ)-catechin and 0.47-2.04% for (2)-epicatechin. The method was suitable for assessing the plasma pharmacokinetics of (þ)-catechin and (2)-epicatechin in rats after their individual oral administration as solutions in either water or milk.