Biomedical subjects

Y S Ho

Publications and source records attributed to Y S Ho.

At least 91 records · Page 5Linked to original sources

PubMed1997

Intracranial meningeal melanocytoma: CT and MRI.

We report the MRI and CT findings of an intracranial meningeal melanocytoma (IMM) arising from Meckel's cave and review the imaging characteristics of IMM. On CT, IMM constantly appear as well-circumscribed, isodense to slightly dense, extra-axial tumours with homogeneous contrast enhancement. This appearance is non-specific and similar to that of meningiomas or small neuromas. On MRI, the signal of IMM is strongly related to the amount of melanin pigment: the more melanin, the more shortening of T1 and T2 relaxation times. Only when it shows as a homogeneous mass, bright on T1 and dark on T2 weighting, can a specific diagnosis of a melanin-containing tumour be made. However, this still cannot provide a distinction between IMM and malignant meningeal melanoma.

Adult↗

PubMed1997

Stability of curcumin in buffer solutions and characterization of its degradation products.

The degradation kinetics of curcumin under various pH conditions and the stability of curcumin in physiological matrices were investigated. When curcumin was incubated in 0.1 M phosphate buffer and serum-free medium, pH 7.2 at 37 degrees C, about 90% decomposed within 30 min. A series of pH conditions ranging from 3 to 10 were tested and the result showed that decomposition was pH-dependent and occurred faster at neutral-basic conditions. It is more stable in cell culture medium containing 10% fetal calf serum and in human blood; less than 20% of curcumin decomposed within 1 h, and after incubation for 8 h, about 50% of curcumin is still remained. Trans-6-(4'-hydroxy-3'-methoxyphenyl)-2,4-dioxo-5-hexenal was predicted as major degradation product and vanillin, ferulic acid, feruloyl methane were identified as minor degradation products. The amount of vanillin increased with incubation time.

Antioxidants↗

PubMed1997

The Colorectal Cancer Recurrence Support (CARES) System.

Colorectal cancer has risen in incidence to become the second commonest form of cancer in Singapore. The primary treatment is surgery but up to 50% of patients still suffer from recurrence of the cancer after surgery. Early identification of recurrence will increase the effectiveness of therapy and the survival of patients. This paper describes the CARES (Cancer Recurrence Support) System, whose objective is to predict the recurrence of colorectal cancer, using Case-based Reasoning (CBR), and supported by other techniques such as data mining and natural language processing. The CARES System employs CBR to compare and contrast between the new and past colorectal cancer patient cases, and makes inferences based on those comparisons to determine the high risk patient groups. The features and functionality of the system are described.

Artificial Intelligence↗

PubMed1997

Overexpression of cellular glutathione peroxidase does not affect expression of plasma glutathione peroxidase or phospholipid hydroperoxide glutathione peroxidase in mice offered diets adequate or deficient in selenium.

Selenium-dependent cellular glutathione peroxidase (GPX1) overexpressing [GPX1(+)] mice were derived by microinjecting a 5.3-kb cloned entire mouse GPX1 genomic DNA into fertilized eggs. The objective of this study was to determine the effect of GPX1 overexpression and dietary selenium on the expression of selenoperoxidases and the status of lipid peroxidation of these transgenic animals. An experiment with a 2 x 2 factorial arrangement of treatments with 15 GPX1(+) and 15 control mice (2 mo old) was conducted for 8 wk. Ten mice of each group (half males and females) were fed a Se-deficient, Torula yeast basal diet (0.02 mg Se/kg, no supplemental vitamin E) and five mice (three males and two females) were fed the basal diet supplemented with 0.51 mg Se/kg as Na2SeO3. The GPX1(+) mice had greater GPX1 activities (one- to sixfold, P < 0.0001) than the control mice at both levels of dietary selenium in all tissues except for liver, in which such difference (100%, P < 0.05) was observed only in Se-deficient mice. The GPX1 mRNA level in kidney and in lung of the Se-deficient GPX1(+) mice was 81% and 7.5-fold greater (P < 0.003) than the respective control level. Overexpression of GPX1 did not alter phospholipid hydroperoxide glutathione peroxidase (GPX4) activities and mRNA levels or glutathione S-transferase (GST) activities in most of the tissues, plasma glutathione peroxidase (GPX3) activity or plasma Se concentrations. No differences in lipid peroxidation in kidney, lung or intestine were observed between the Se-deficient GPX1(+) and control mice. In conclusion, the overexpression of the GPX1 gene in these mice was tissue specific and did not affect the expression of GPX3, GPX4 or GST and plasma Se levels; dietary Se appeared to affect the GPX1 overexpression at its mRNA level.

Animals↗

PubMed1997

Cellular glutathione peroxidase knockout mice express normal levels of selenium-dependent plasma and phospholipid hydroperoxide glutathione peroxidases in various tissues.

Selenium-dependent cellular glutathione peroxidase (GPX1) knockout [GPX1(-)] mice were derived from 129/SVJ x C57BL/6 hybrid mice by microinjecting C57BL/6 blastocysts with recombinant embryonic stem cells carrying a target mutation in the GPX1 gene. Experiment 1 was conducted to determine the effects of the GPX1 knockout on the susceptibility of mice to dietary vitamin E and Se deficiency and on the expression of the Se-dependent plasma glutathione peroxidase (GPX3) and phospholipid hydroperoxide glutathione peroxidase (GPX4), and the Se-independent glutathione S-transferase (GST). Eleven GPX1(-) and 11 control mice (5 wk old, six males and five females) were fed a Se-deficient, Torula yeast basal diet (0.02 mg Se/kg, no supplemental vitamin E) or the basal diet supplemented with 0.5 mg Se/kg (as Na2SeO3) for 13 wk. Experiment 2 was conducted to determine the effect of the GPX1 knockout on the total Se concentration in the liver of Se-adequate mice. Six GPX1(-) and four control mice (5 wk old, half males and females) were fed the basal diet supplemented with 0.2 mg Se/kg and 15 mg of all-rac-alpha-tocopheryl acetate/kg for 5 wk. There was no difference in body weight gain or apparent susceptibility to dietary vitamin E and Se deficiency between the GPX1(-) and control mice. Knockout of GPX1 resulted in almost complete abolishment of GPX1 activity in various tissues, but had no effect on the GPX3 or GPX4 mRNA level and activity or the GST activity in several tissues at either level of dietary Se. The liver total Se concentration in the Se-adequate GPX1(-) mice was only 42% of that in the controls (P < 0. 0001). These results indicate that GPX1 is expressed independently of GPX3 or GPX4 and represents approximately 60% of the total hepatic Se in Se-adequate mice.

Animals↗

PubMed1997

Peroxide-induced damage in lenses of transgenic mice with deficient and elevated levels of glutathione peroxidase.

Transgenic mice with elevated glutathione peroxidase (GSHPx) activity and gene knockout animals with a deficiency of the enzyme were used to investigate the role of GSHPx in defending the lens against H2O2-induced damage. The effects of peroxide on cultured lenses were determined by using light and transmission electron microscopy to evaluate morphological changes occurring in the epithelium and superficial cortex of the central and equatorial regions of the lens. DNA single-strand breaks in the epithelium were also examined. Following a 30-min exposure to 25 microM H2O2, lenses from normal animals showed distinct changes in the morphology of both the epithelium and superficial cortex. The damage to these cells was extensive in lenses of gene knockout mice in which activity of GSHPx was undetectable. In marked contrast, lenses of transgenic mice, which had 5-fold higher activities of GSHPx, were able to resist the cytotoxic effects. Similar to damage to cell morphology, the extent of DNA strand breaks was significantly lower (40% of control) in H2O2-exposed lenses as compared to normal lenses while DNA damage in gene knockout lenses was 5 times greater than that of GSHPx-rich transgenic lenses. The present studies extend our previous findings on the role of the glutathione redox cycle in the detoxification of peroxide and demonstrate that an increase in GSHPx activity protects the lens against peroxide-induced changes in cell morphology and DNA strand breaks.

Animals↗

PubMed1997

Immunohistochemical analysis of insulin-like growth factor I, insulin-like growth factor I receptor and insulin-like growth factor II in endometriotic tissue and endometrium.

BACKGROUND: The purpose of this study was to investigate unprecedentedly immunohistochemical localization of insulin-like growth factor I, insulin-like growth factor I receptor and insulin-like growth factor II in endometriotic tissue, and to compare staining intensity with that of endometrium obtained simultaneously. METHODS: Endometriotic and corresponding endometrial tissue samples were obtained during operative laparoscopy from eighteen infertile patients for the problem of infertility. Semiquantitative scoring was used for analysis of results. RESULTS: It was demonstrated that insulin-like growth factor I and insulin-like growth factor I receptor were present in both endometriotic and endometrial tissues. In contrast, there was little insulin-like growth factor II present in either ectopic or eutopic endometrial tissue. For insulin-like growth factor I and insulin-like growth factor I receptor, the immunostaining score was similar between ectopic and eutopic endometrial tissues. There was no significant difference in immunostaining score between glandular epithelium and stromal cells. CONCLUSIONS: insulin-like growth factor I and insulin-like growth factor I receptor could be demonstrated immunohistochemically in both endometriotic and endometrial tissues.

Adult↗

PubMed1997

Skull metastasis with brain invasion from thyroid papillary microcarcinoma.

Thyroid papillary microcarcinoma has a notably benign clinical course among carcinomas. The occurrence of distant metastases is exceptional, but significantly increases the risk of mortality. We report the case of a 75-year-old woman with a 1.0 cm primary thyroid papillary microcarcinoma with skull metastases and brain invasion. The clinical presentation was a large mass over the occipital area which progressively grew over the course of 1 year. No thyroid nodule or lymph nodes were palpable. The metastatic mass and primary tumor were surgically removed. The serum thyroglobulin level was 163 ng/mL 1 month after surgery. There was no further management because the patient refused follow-up. She returned to the hospital 15 months later due to a seizure. The tumor had further extended into the brain tissue. Her condition progressively deteriorated and she died 2 months later due to uncontrollable seizures.

Aged↗

PubMed1997

Cerebral sparganosis: increased uptake of technetium-99m-HMPAO.

Cerebral sparganosis is an extremely rare intracranial parasitic infectious disease. We report findings of 99mTc-HMPAO cerebral perfusion SPECT in a case with cerebral sparganosis. SPECT revealed an irregularly shaped area with markedly increased 99mTc-HMPAO uptake in the parasitic infectious region of the cerebrum. Both white and gray matter was involved, the white matter involved predominantly. Decreased perfusion to the right cerebellum, suggesting cross cerebellar diaschisis, was also demonstrated. This article illustrates that cerebral sparganosis is one of the causes of increased 99mTc-HMPAO uptake in the cerebrum and should be considered clinically if present.

Aged↗

PubMed1997

Suppression of nitric oxide-induced apoptosis by N-acetyl-L-cysteine through modulation of glutathione, bcl-2, and bax protein levels.

It has been demonstrated that nitric oxide (NO) can promote apoptosis in human cancer cells. To test the protective effects of antioxidants (N-acetyl-L-cysteine (LNAC) and free-radical spin traps (5,5-dimethyl-1-pyrroline N-oxide and 2,2,6,6,-tetramethyl-1-piperidinyloxy) against NO-induced apoptosis, a human colon cancer cell line (COLO 205) was treated with NO, and its survival rate was evaluated both with and without antioxidant therapy. LNAC arrested the development of progression of apoptosis in COLO 205 cells in a dose-dependent manner, promoted long-term survival, and prevented the internucleosomal DNA cleavage induced by NO. The intracellular level of glutathione (GSH) was found to be elevated in cells after exposure to LNAC. The bax protein levels were elevated by NO treatment, and this effect was blocked by LNAC. On the other hand, the bcl-2 oncoprotein level in the LNAC-pretreated cells was significantly elevated in a time-dependent manner compared to cells that received NO pretreatment. In summary, our results suggest that the protective effect of LNAC may be linked to its inducement of increases in cellular GSH and bcl-2 protein levels and to its suppression of cellular bax protein in treated cells.

Acetylcysteine↗

PubMed1997

Expression and chromosomal mapping of mouse Gpx2 gene encoding the gastrointestinal form of glutathione peroxidase, GPX-GI.

GPX-GI is a cytosolic tetrameric Se-dependent glutathione peroxidase, similar in properties to GPX-1. Unlike the almost ubiquitous GPX-1, GPX-GI is mainly expressed in the epithelium of gastrointestinal tract. GPX-GI contributes to at least fifty percent of GPX activity in rodent small intestinal epithelium. The total GPX activity consists of at least 70% of selenium-dependent GPX activity in this compartment. By analyzing a panel of mouse interspecies DNA from the Jackson Laboratory's backcross resource, we mapped Gpx2 gene to mouse chromosome 12 between D12Mit4 and D12Mit5, near the Ccs1 locus which contains a colon cancer susceptibility gene. A pseudogene, Gpx2-ps is mapped to mouse chromosome 7. Comparison of Gpx2 gene expression in three pairs of C57BL/6Ha and ICR/Ha mice which are respectively resistant and sensitive to dimethylhydrazine-induced colon cancer, we found a higher Gpx2 mRNA level in C57BL/6Ha colon than ICR/Ha colon. Interestingly, a lower level of GPX activity is found in the resistant strain of mice. Because GPX-1 has three times higher specific activity than GPX-GI, our data suggest that the decreased GPX activity may result from a higher level of Gpx2 gene expression in those cells co-express Gpx1 gene.

Amino Acid Sequence↗

PubMed1997

Primary diffusely infiltrative adenocarcinoma of the colon and rectum.

BACKGROUND: Primary diffusely infiltrative colorectal adenocarcinoma is rare. About 100 cases have been reported in the literature. The mucosal alterations in this type of tumor and their clinicopathological characteristics in relation to survival are not clear. METHODS: We retrospectively reviewed 30 cases of primary diffusely infiltrative colorectal adenocarcinoma operated upon in a single institution. RESULTS: Eighteen (60%) of these 30 patients were women. The average age at diagnosis was 47.4 (SD, 19.3) years. Eighteen tumors (60%) were located in the rectum. The tumors could be classified into two major types. A type 1 tumor had minimal mucosal alteration and no discrete ulcer. A type 2 tumor was associated with a discrete ulcer. The type 1 tumor was more frequently associated with intracellular or extracellular mucin production and stage IV disease. Hematogenous spread (including peritoneal carcinomatosis) was more frequently seen in type 1 than in the type 2 tumors (61% vs. 18%, p = 0.013). The overall median cancer-specific survival time was 15 (SE, 3; 95% confidence interval, 10-21) months. TNM stage is the only significant factor in predicting outcome (p = 0.016). When compared with stages II and III, the odds of death for stage IV was 2.9 (95% confidence interval: 1.1-7.4). CONCLUSION: Diffusely infiltrative colorectal cancer can be separated into two subtypes according to the presence of a discrete ulcer. The type 1 tumor (without a discrete ulcer) was associated with a higher frequency of hematogenous spread. TNM Stage was the only important clinicopathological factor in determining outcome.

Adenocarcinoma↗

PubMed1996

The protective role of manganese superoxide dismutase against adriamycin-induced acute cardiac toxicity in transgenic mice.

Adriamycin (ADR) is a potent anticancer drug known to cause severe cardiac toxicity. Although ADR generates free radicals, the role of free radicals in the development of cardiac toxicity and the intracellular target for ADR-induced cardiac toxicity are still not well understood. We produced three transgenic mice lines expressing increased levels of human manganese superoxide dismutase (MnSOD), a mitochondrial enzyme, as an animal model to investigate the role of ADR-mediated free radical generation in mitochondria. The human MnSOD was expressed, functionally active, and properly transported into mitochondria in the heart of transgenic mice. The levels of copper-zinc SOD, catalase, and glutathione peroxidase did not change in the transgenic mice. Electron microscopy revealed dose-dependent ultrastructural alterations with marked mitochondrial damage in nontransgenic mice treated with ADR, but not in the transgenic littermates. Biochemical analysis indicated that the levels of serum creatine kinase and lactate dehydrogenase in ADR-treated mice were significantly greater in nontransgenic than their transgenic littermates expressing a high level of human MnSOD after ADR treatment. These results support a major role for free radical generation in ADR toxicity as well as suggesting mitochondria as the critical site of cardiac injury.

Animals↗

PubMed1996

p53 gene mutation in cerebral primitive neuroectodermal tumor in Taiwan.

p53 mutation has been rarely reported in cerebral primitive neuroectodermal tumors (PNET). To determine the significance of p53 mutations in the development of cerebral PNET, we studied cerebral PNET samples from 14 patients, 8 females and 6 males with a mean age of 38 years (range 10 months to 77 years) who had total or subtotal surgical resection. Histological typing of PNET with neuronal (N) and non-neuronal (NN) differentiation groups revealed 8 and 6 cases, respectively. Six (43%) of the 14 patients had p53 mutation. The p53(+) and p53(-) groups had an age range of 19-77 with a mean of 49 years and 10 months to 57 years with a mean of 30 years, respectively. p53 expression between the PNET-N and PNET-NN groups was 5 of 8 (62.5%) and 1 of 6 (16.7%), respectively. The mutations contained 3 transitions, 2 transversions and 1 frameshift; none of them occurred at the site of 'hot-spot' residues (codons 175, 248, 273). The results suggest that: (1) p53 mutation in cerebral PNET tends to show a higher incidence of neuronal differentiation and occurs in the older age group in Taiwan, (2) there was no difference in survival time between the PNET-N and PNET-NN groups (7 months and 6 months) (P = 0.54), and between p53(+) and p53(-) groups (6 months and 7 months) (P = 0.57), and (3) PNET may be an entity of a heterogenous group of tumors with different genetic mechanisms controlling their trends of differential lineage. Further studies are needed to determine the significance of p53 mutations in PNET development, especially the role of carcinogens in the genesis of PNET in Taiwan.

Adolescent↗

PubMed1996

p53 gene mutation in thyroid carcinoma.

The pattern of p53 protein expression was examined in 92 cases of thyroid carcinoma. When the cases were divided into two groups with regard to their cytoplasmic staining only or nucleus staining only, the frequency of the nucleus staining group was significantly higher in the poorly differentiated carcinoma (PDC) and undifferentiated carcinoma (UDC) groups (10.5% and 25%) compared with the other groups of histologic subtype (0%). The results suggest positivity in nucleus staining for p53 may be a marker for the biologically worse carcinomas, PDC and UDC, however, tumors showing only cytoplasmic staining of p53 favor a fair prognosis. In this paper, we also elucidate the spectrum of genotypic aberrations of p53 in each histological subtype. Of 92 thyroid tumor samples analyzed, the overall frequency of p53 mutation was 8.5%. The mutations occurred in 4.35% (2/46) ot WDC, 17.2% (5/29) of PDC, and 16.7% (1/6) of oncocytic carcinoma. Two of five PDC cases and one papillary carcinoma revealed point mutations in exon 8 as follows; GTG (val) to CTG (leu) at codon 272 in case 23T, CGA (arg) to CCA (pro) at codon 306 in case of 30T, and CGG (arg) to AGG (arg) at codon 282 in case 28T. All of the p53 mutations detected were represented by single nucleotide changes including two missense and one silent mutation. In contrast to the missense mutations found in PDC, it is interesting to note that the silent mutation was checked in 28T of well differentiated papillary carcinoma. These results represents molecular evidence that p53 gene aberration associated with overexpression of the mutant form of p53 protein plays a crucial role in the biologically aggressive subtypes of thyroid carcinoma, and point mutation only was not sufficient to be a prognostic marker for the biologically aggressive malignancy of thyroid tumors. There was no p53 gene aberration found in four cases of undifferentiated carcinoma (UDC) studied. The results suggest that other unknown factors should be responsible for the aggressiveness in some UDC of thyroid carcinoma except overexpression of p53.

Carcinoma↗

PubMed1996

Establishment of xenografts and cell lines from well-differentiated human thyroid carcinoma.

BACKGROUND: Our aim was to establish Chinese human thyroid cancer cell lines and to provide the material for thyroid cancer research. METHODS: We collected thyroid cancer tissues from 93 patients with thyroid cancer for developing the primary culture. Thyroid cancer tissues were verified by frozen sections during the operations, then subjected to primary cell culture. During the first several passages, fibroblasts were removed by selective attachment. RESULTS: From the 93 cancer tissues used, two follicular cancer tissues from the metastatic area (CGTH W-1, CGTH W-2) and one papillary thyroid cancer tissue (CGTH W-3) could be passed over 50 times. Cellular transformation with loss of contact inhibition occurred during passages 5-8. Electron microscopic studies of the CGTH W-1 cell line showed the presence of an abundance of mitochondria and Golgi complex. Presence of microvilli with interdigitations between neighboring cells were found in CGTH W-2 and CGTH W-3 cell lines. Severe combined immunodeficient (SCID) mice were used to determine whether these cells were tumorigenic. Two months after transplantation of 1 x 10(7) CGTH W-1, 2, and 3 cells into SCID mice, subcutaneous tumors approximately 2-2.5 cm in size were clearly visible. After affinity cross-linking an IGF-I with insulin-like growth factor binding proteins complex corresponding to a molecular size of 41 kDa was observed in culture media collected from CGTH W-1, SW 579, and RO82 W-1 cells. CONCLUSIONS: Three thyroid cancer cell lines were established, which may provide material for future thyroid cancer research.

Animals↗

PubMed1996

Induction of p53 and p21/WAF1/CIP1 expression by nitric oxide and their association with apoptosis in human cancer cells.

In this study, human and rat cancer cells were used to investigate the expression of p53 and p21/WAF1/CIP1 and their association with apoptosis after exposure to nitric oxide (NO). It was found that NO induced nuclear accumulation of p53 protein in a dose- and time-dependent manner. The level of p53 protein was elevated by about fivefold compared with that of mock-treated cells 48 h after exposure to 300 ppm NO. The induction of p53 by NO was found by pulse-chase analysis to be mainly regulated by post-translational modification. The correlation between p53 status and apoptosis induced by NO in human cancer cells was also investigated in this study. We found that apoptosis was easily induced in cells containing wild-type p53 (COLO 205 and Hep G2) after exposure to NO. The p21/WAF1/CIP1 protein was induced by NO in cells containing wild-type p53 (Hep G2) but not in cells without p53 (Hep 3B) or with mutated p53 (HT-29). Our results indicate that wild-type p53 and p21/WAF1/CIP1 expression was elevated in human cancer cells by exposure to NO and suggest that this may eventually promote apoptosis.

3T3 Cells↗

PubMed1996

Variation in cellular glutathione peroxidase activity in lens epithelial cells, transgenics and knockouts does not significantly change the response to H2O2 stress.

This investigation examines the contribution of glutathione peroxidase (GSHPx-1) in degrading H2O2 in lens preparations. Rabbit (N/N1003A) and normal and GSHPx-1 transfected mouse (alpha TN4-1) lens epithelial cell lines and normal and GSHPx-1 transgenic and knockout mouse lenses were utilized. GSHPx-1 activity in the cell lines was increased from two-fold to about four-fold, in the lenses from transgenics more than four-fold and the lenses from knockouts had less than 3% of normal GSHPx-1 activity. The transgenic and knockout mice as well as their lenses appeared normal for up to 3 to 4 months, the longest period of observation. The preparations were subjected to oxidative stress by placing them either in a medium containing 120 or 300 microM H2O2 or utilizing photochemical stress where the H2O2 levels normally rise to about 100 microM over a few hours in the presence of a normal lens. With all preparations, it was found that either markedly increasing or eliminating GSHPx-1 activity had only a small effect on the system's ability to metabolize H2O2, 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU), an inhibitor of GSSG reductase (GSSG Red) and 3-aminotriazole (3-AT), an inhibitor of catalase, also had little effect. However, the addition of both inhibitors caused a marked decrease in H2O2 degradation. Examination of the distribution of GSHPx-1 in the lens indicated that the activity per milligram of protein was evenly distributed between the epithelium and the remainder of the lens in the normal lens and was about 1.7-fold greater in the epithelium of transgenic lenses than in the remainder of the lens. Surprisingly, the distribution of GSSG Red was quite different with eight- to ten-fold more activity in the epithelium. Catalase was also found to be concentrated in the epithelium. With H2O2 exposure, a rapid loss of non-protein thiol (NP-thiol) was found in cell cultures and in the epithelia of cultured lenses. However, the remainder of the lens showed little change in NP-thiol. The variation of GSHPx-1 activity did not influence the NP-thiol changes which occurred more rapidly and to a greater extent in the presence of BCNU. The addition of BCNU also caused a decrease in total lens NP-thiol. Examination of thymidine incorporation and choline transport, indicators of nuclear and membrane function, also reflects the H2O2 degradation data, showing little difference in the degree to which H2O2 effects these parameters in lenses from normal and transgenic animals. Catalase activity is four- to six-fold greater than GSHPX-1 activity in the alpha TN4-1 cell lines, about three-fold lower in the rabbit cell line and, remarkably, about 18-fold lower than the peroxidase in the normal mouse lens. In spite of such observations, the consistent overall conclusion is that GSHPx-1 and catalase function together but when GSHPx-1 is knocked out or GSSG Red is inhibited, catalase is able to protect the system from H2O2 stress. Indeed, the young mouse does not appear to require GSH Px-1 for normal function.

Animals↗