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With 3 plates and 2 figures in the text)We define the species boundaries of white-toothed shrews (genus Crocidura) in Taiwan using karyological and morphological characteristics. Ninety-nine animals were obtained from all over Taiwan at capture rates usually less than 10%. Three species are recognized by distinct cytotypes:Crociduru uttenuata tanakae 2n = 40, FN = 56; Crocidura suaveolens hoslefti 2n = 40, FN = 50; Crocidura kurodai 2n = 40, FN = 54. A suite of six morphological characters diagnose the three species: shape of skull, position of incisive foramina, shape of fourth upper premolar, shape of pinna, tail vibrissae, and foot pads. A species key and notes on the life history of each species are provided. Finally, we discuss chromosomal evolution and biogeography of Crociduru in East and South East Asia.

Nickel has been shown to inhibit DNA repair in a way that may play a role in its toxicity. Since nickel treatment increases cellular reactive oxygen species (ROS), we have investigated the involvement of ROS in nickel inhibition of DNA repair. Inhibition of glutathione synthesis or catalase activity increased the enhancing effect of nickel on the cytotoxicity of ultraviolet (UV) light. Inhibition of catalase and glutathione peroxidase activities also enhanced the retardation effect of nickel on the rejoining of DNA strand breaks accumulated by hydroxyurea plus cytosine-beta-D-arabinofuranoside in UV-irradiated cells. Since DNA polymerization and ligation are involved in the DNA-break rejoining, we have investigated the effect of ROS on these two steps in an extract of Chinese hamster ovary cells. Nickel inhibition of the incorporation of (3H)dTTP into the DNase I-activated calf thymus DNA was stronger than the ligation of poly(dA) x oligo(dT), whereas H2O2 was more potent in inhibiting DNA ligation than DNA polymerization. Nickel, in the presence of H2O2, exhibited a synergistic inhibition on both DNA polymerization and ligation and caused protein fragmentation. In addition, glutathione could completely recover the inhibition by nickel or H2O2 alone but only partially recover the inhibition by nickel plus H2O2. Therefore, nickel may bind to DNA-repair enzymes and generate oxygen-free radicals to cause protein degradation in situ. This irreversible damage to the proteins involved in DNA repair, replication, recombination, and transcription could be important for the toxic effects of nickel.

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The growth of tissue culture TO-2 cells derived from the warm water fish Tilapia, the induction of thermotolerance, and protein synthesis profiles of these cells in response to temperature changes were examined. TO-2 cells can grow between 15 to 34 degrees, with an optimal growth temperature of 31 degrees. There is no apparent killing of the cells when the temperature is lowered to 4 degrees for up to 3 days. Survival of TO-2 cells at 43 degrees was studied after various preheat treatments: 1) acute heating at 40 degrees for 15 min followed by 31 degrees incubation, 2) chronic exposure at 37 degrees for several hr, or 3) long-term thermal adaptation at 34 degrees. The cells acquire thermotolerance from pre-exposure to 37 degrees for as short as 6 hr. Preheating at 40 degrees followed by incubation at 31 degrees also induces thermotolerance against a subsequent 43 degrees heat challenge. In addition, 34 degrees thermal adapted cells are resistant to 43 degrees heating. One- and two-dimensional gel electrophoresis of proteins after heat treatments show that three major heat shock proteins with molecular weights around 87, 70, and 27 kD are preferentially synthesized. The synthesis of two additional proteins with an isoelectric point of 6.9 and molecular weights of 60 and 44 kD are significantly enhanced in 34 degrees thermal-adapted and 37 degrees chronic heated cells, but not in cells subjected to an acute heat shock at either 40 degrees or 43 degrees. On the other hand, the 27 kD heat shock proteins are mainly present in the 43 degrees, 40 degrees, and 37 degrees heat-shocked cells, but not in the 34 degrees thermal-adapted cells.