Olfactory morphology of carcharhinid and sphyrnid sharks: Does the cephalofoil confer a sensory advantage?

Many hypotheses have been advanced to explain the adaptive significance of the sphyrnid cephalofoil, including potential advantages of spacing the olfactory organs at the distal tips of the broad surface. We employed comparative morphology to test whether the sphyrnid cephalofoil provides better stereo-olfaction, increases olfactory acuity, and samples a greater volume of the medium compared to the situation in carcharhiniform sharks. The broadly spaced nares provide sphyrnid species with a significantly greater separation between the olfactory rosettes, which could lead to an enhanced ability to resolve odor gradients. In addition, most sphyrnid species possess prenarial grooves that greatly increase the volume of water sampled by the nares and thus increase the probability of odorant encounter. However, despite a much greater head width, and a significantly greater number of olfactory lamellae, scalloped hammerhead sharks do not possess a greater amount of olfactory epithelial surface area than the carcharhiniform sandbar sharks. Therefore, sphyrnid sharks might not possess any greater olfactory acuity than carcharhinids. Despite this, there are clear olfactory advantages to the cephalofoil head morphology that could have led to its evolution, persistence, and diversification. persistence, and diversification.     

Limb chondrogenesis of the seepage salamander, Desmognathus aeneus (amphibia: plethodontidae)

Salamanders are infrequently mentioned in analyses of tetrapod limb formation, as their development varies considerably from that of amniotes. However, urodeles provide an opportunity to study how limb ontogeny varies with major differences in life history. Here we assess limb development in Desmognathus aeneus, a direct-developing salamander, and compare it to patterns seen in salamanders with larval stages (e.g., Ambystoma mexicanum). Both modes of development result in a limb that is morphologically indistinct from an amniote limb. Developmental series of A. mexicanum and D. aeneus were investigated using Type II collagen immunochemistry, Alcian Blue staining, and whole-mount TUNEL staining. In A. mexicanum, as each digit bud extends from the limb palette Type II collagen and proteoglycan secretion occur almost simultaneously with mesenchyme condensation. Conversely, collagen and proteoglycan secretion in digits of D. aeneus occur only after the formation of an amniote-like paddle. Within each species, Type II collagen expression patterns resemble those of proteoglycans. In both, distal structures form before more proximal structures. This observation is contrary to the proximodistal developmental pattern of other tetrapods and may be unique to urodeles. In support of previous findings, no cell death was observed during limb development in A. mexicanum. However, apoptotic cells that may play a role in digit ontogeny occur in the limbs of D. aeneus, thereby suggesting that programmed cell death has evolved as a developmental mechanism at least twice in tetrapod limb evolution.     

Antioxidant mechanism of heme oxygenase-1 involves an increase in superoxide dismutase and catalase in experimental diabetes

Increased heme oxygenase (HO)-1 activity attenuates endothelial cell apoptosis and decreases superoxide anion (O2-) formation in experimental diabetes by unknown mechanisms. We examined the effect of HO-1 protein and HO activity on extracellular SOD (EC-SOD), catalase, O2-, inducible nitric oxide synthase (iNOS), and endothelial nitric oxide synthase (eNOS) levels and vascular responses to ACh in control and diabetic rats. Vascular EC-SOD and plasma catalase activities were significantly reduced in diabetic compared with nondiabetic rats (P < 0.05). Upregulation of HO-1 expression by intermittent administration of cobalt protoporphyrin, an inducer of HO-1 protein and activity, resulted in a robust increase in EC-SOD but no significant change in Cu-Zn-SOD. Administration of tin mesoporphyrin, an inhibitor of HO-1 activity, decreased EC-SOD protein. Increased HO-1 activity in diabetic rats was associated with a decrease in iNOS but increases in eNOS and plasma catalase activity. On the other hand, aortic ring segments from diabetic rats exhibited a significant reduction in vascular relaxation to ACh, which was reversed with cobalt protoporphyrin treatment. These data demonstrate that an increase in HO-1 protein and activity, i.e., CO and bilirubin production, in diabetic rats brings about a robust increase in EC-SOD, catalase, and eNOS with a concomitant increase in endothelial relaxation and a decrease in O2-. These observations in experimental diabetes suggest that the vascular cytoprotective mechanism of HO-1 against oxidative stress requires an increase in EC-SOD and catalase.     

Late preconditioning induced by NO donors, adenosine A1 receptor agonists, and delta1-opioid receptor agonists is mediated by iNOS

Although ischemia-induced late preconditioning (PC) is known to be mediated by inducible nitric oxide (NO) synthase (iNOS), the role of this enzyme in pharmacologically induced late PC remains unclear. We tested whether targeted disruption of the iNOS gene abrogates late PC elicited by three structurally different NO donors [diethylenetriamine/NO (DETA/NO), nitroglycerin (NTG), and S-nitroso-N-acetyl-penicillamine (SNAP)], an adenosine A1 receptor agonist [2-chloro-N6-cyclopentyladenosine (CCPA)], and a delta1-opioid receptor agonist (TAN-670). The mice were subjected to a 30-min coronary occlusion followed by 24 h of reperfusion. In iNOS knockout (iNOS-/-) mice, infarct size was similar to wild-type (WT) controls, indicating that iNOS does not modulate infarct size in the absence of PC. Pretreatment of WT mice with DETA/NO, NTG, SNAP, TAN-670, or CCPA 24 h before coronary occlusion markedly reduced infarct size. In iNOS-/- mice, however, the late PC effect elicited by DETA/NO, NTG, SNAP, TAN-670, and CCPA was completely abrogated. Furthermore, in WT mice pretreated with TAN-670 or CCPA, the selective iNOS inhibitor 1400W also abolished the delayed PC properties of these drugs; 1400W had no effect in WT mice. These data demonstrate that iNOS plays an obligatory role in NO donor-induced, adenosine A1 receptor agonist-induced, and delta1-opioid receptor agonist-induced late PC, underscoring the critical role of this enzyme as a common mediator of cardiac adaptations to stress.     

Fibroblast cell lines from young adult mice of long-lived mutant strains are resistant to multiple forms of stress

Previous studies have shown that dermal fibroblast cell lines derived from young adult mice of the long-lived Snell dwarf mutant stock are resistant, in vitro, to the cytotoxic effects of H(2)O(2), cadmium, UV light, paraquat, and heat. We show here that similar resistance profiles are seen in fibroblast cells derived from a related mutant, the Ames dwarf mouse, and that cells from growth hormone receptor-null mice are resistant to H(2)O(2), paraquat, and UV but not to cadmium. Resistance to UV light, cadmium, and H(2)O(2) are similar in cells derived from 1-wk-old Snell dwarf or normal mice, and thus the resistance of cell lines derived from young adult donors reflects developmental processes, presumably hormone dependent, that take place in the first few months of life. The resistance of cells from Snell dwarf mice to these stresses does not reflect merely antioxidant defenses: dwarf-derived cells are also resistant to the DNA-alkylating agent methyl methanesulfonate. Furthermore, inhibitor studies show that fibroblast resistance to UV light is unaffected by the antioxidants ascorbic acid and N-acetyl-L-cysteine. These data suggest that postnatal exposure to altered levels of pituitary hormones leads to development of cellular resistance to oxidative and nonoxidative stressors, which are stable through many rounds of in vitro cell division and could contribute to the remarkable disease resistance of long-lived mutant mice.