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Not AvailableDiel cyclic hypoxia occurs with varying frequency and duration in freshwater habitats, yet little is known about its effects on reproduction of freshwater fishes. The present study shows that long-term exposure of goldfish (Carassius auratus) to cyclic hypoxia (0.8 ± 0.2 mg/l dissolved oxygen) for 9 h or more, per day, altered plasma lipid and sex steroid profiles, which in turn directly or indirectly suppressed ovarian growth and viable spermatozoa production. Hypoxia decreased total cholesterol and high density lipoprotein (HDL p < 0.05) and elevated triglycerides (TG; p < 0.05) in both sexes. Plasma steroid concentrations particularly of 17α-hydroxyprogesterone (17-HP), estradiol (E2), testosterone (T) in females, and T and 11-ketotestosterone (11-KT) in males were attenuated under diel hypoxic conditions. Intriguingly, both diel and continuous hypoxia elevated plasma E2 and vitellogenin levels in males. However, neither lipid nor steroid profiles recorded any variation in a dose-dependent manner in response to diel hypoxia. The reduced GSI, decreased number of tertiary oocytes, and motile spermatozoa in hypoxic fish clearly indicate suppression of gametogenesis. Thereby, prolonged diel cyclic hypoxia may affect valuable fishery resources and fish population structure by impairing reproductive performances and inducing estrogenic effects in males.Not Availabl

p53 dependent apoptotic cell death induces embryonic malformation in Carassius auratus under chronic hypoxia.

Hypoxia is a global phenomenon affecting recruitment as well as the embryonic development of aquatic fauna. The present study depicts hypoxia induced disruption of the intrinsic pathway of programmed cell death (PCD), leading to embryonic malformation in the goldfish, Carrasius auratus. Constant hypoxia induced the early expression of pro-apoptotic/tumor suppressor p53 and concomitant expression of the cell death molecule, caspase-3, leading to high level of DNA damage and cell death in hypoxic embryos, as compared to normoxic ones. As a result, the former showed delayed 4 and 64 celled stages and a delay in appearance of epiboly stage. Expression of p53 efficiently switched off expression of the anti-apoptotic Bcl-2 during the initial 12 hours post fertilization (hpf) and caused embryonic cell death. However, after 12 hours, simultaneous downregulation of p53 and Caspase-3 and exponential increase of Bcl-2, caused uncontrolled cell proliferation and prevented essential programmed cell death (PCD), ultimately resulting in significant (p<0.05) embryonic malformation up to 144 hpf. Evidences suggest that uncontrolled cell proliferation after 12 hpf may have been due to downregulation of p53 abundance, which in turn has an influence on upregulation of anti-apoptotic Bcl-2. Therefore, we have been able to show for the first time and propose that hypoxia induced downregulation of p53 beyond 12 hpf, disrupts PCD and leads to failure in normal differentiation, causing malformation in gold fish embryos

Population parameters of the catfishes, <i>Arius caelatus </i>(Valenciennes, 1830) and <i>Arius tenuispinis </i>(Day, 1877) from Mumbai waters

775-780The population parameters like growth, mortality, exploitation rate and length at first capture of Arius caelatus and A. tenuispinis from Mumbai waters were investigated to derive information required for their management. Asymptotic length (L∞) and growth coefficient (K) were calculated as 520 mm and 0.70 year-1 for A. caelatus and <span style="mso-ansi-language: EN-IN">550 mm and 0.73 year-1 for A. tenuispinis, respectively. Instantaneous rate of total, natural and fishing mortalities were estimated to be 2.37, 1.18 and 1.19 for A. caelatus and 2.42, 1.19 and 1.23 for A. tenuispinis, respectively. Size at first capture was estimated as 274 mm for A. caelatus and 268 mm for A. tenuispinis. Exploitation ratio (E) was found to be at optimum level for both A. caelatus (0.5) and A. tenuispinis (0.51), indicating the stocks are exploited at optimum level and can be fished sustainably in years to come. </span

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Comparative length-weight relationship of two species of catfishes, <i>Arius caelatus </i>(Valenciennes, 1840) and <i>Arius tenuispinis </i>(Day, 1877) from Mumbai waters⁺

266-269Based on the length weight data collected from New Ferry Wharf (NFW), Sasoon Docks (S.D) & Versova landing centres, the length-weight relationship for two important catfishes, Arius caelatus and A. tenuispinis from Mumbai waters has been reported in the present communication. There is no significant difference in growth between sexes for both the species, based on the ANACOVA test. Length-weight relationship derived were W = 0.00419 * L 3.263 (R2 = 0.899) and W = 0.0306 * L 2.720 (R2 = 0.953), for A. caelatus and <i style="mso-bidi-font-style: normal">A. tenuispinis respectively. Growth pattern study showed isometric growth for A. caelatus and A. tenuispinis.</i

Malformation in gold fish embryos under normoxia and hypoxia.

<p>(A). Viability assay (% of cumulative death): Gold fish embryos showed 100% mortality under anoxia >15 hours and were thus found to be anoxia intolerant. After 144 h, percentages of dead embryos were 95%, 31%, 16% and 12 % in 0.05, 1, 2, and 6 mg/l DO respectively. (B). Malformation (%): After 144 h, percentage of embryos with malformation in hypoxia group was significantly higher (p<0.001) than that of normoxia. (C). Body length: After 144 h, embryos exposed to hypoxia showed significantly (p<0.001) shorter body length than that of control group. (D). Somite Numbers: Highest somite reduction was observed during 12 hpf compared to control. Different superscripts in cumulative death assay indicate significant differences (p<0.05) amongst different treatments and control. Asterisks indicate significant differences between normoxic and hypoxic groups (paired t test, *<i>p</i><0.05 and *** <i>p</i><0.001) at different times. Values are expressed as mean ± SEM (n = 20).</p

Bcl-2 and cell proliferation assay of embryonic cells under normoxia and hypoxia.

<p>(A). Bcl-2 assay: Bcl-2 reached its highest (p<0.05) level in cell lysates during 24 hpf. Bcl-2 expression was not detected in normoxic embryos during embryonic development. (B).Embryonic cell proliferation: Normoxic embryos showed continuous cell proliferation till 24 hpf, whereas hypoxic embryos showed no significant cell proliferation up to 7 hpf (gastrula phase), followed by abrupt increase in proliferation after 7 hpf up to 24 hpf. Different superscripts indicate significant difference (<i>p</i><0.05) amongst normoxic and hypoxic groups at different times. Values are expressed as mean ± SEM (n = 10).</p

Characterization of pattern of cell death and cellular DNA fragmentation.

<p>(A). Type of cell death (Apoptotic or Necrotic): DNA fragments in hypoxic cell lysate significantly increased (<i>p</i><0.05) after 1 h of incubation and reached highest level at 3 h and continued to be high up to 9 h, with a small peak at 6 h. No BrdU labeled DNA fragment was detected in the hypoxic cell supernatants during first 4 hours of incubation, indicating that DNA fragmentation had occurred prior to lysis of plasma membrane; Hence, cause of cell death may be attributed to apoptosis and not due to necrosis, under hypoxia. (B). DNA fragmentation: Phenomena of cellular DNA fragmentation under hypoxia started increasing after blastula (4 hpf) stage and reached its highest (<i>p</i><0.05) during gastrula phase (7 hpf), thereafter returning to the level of control after 12 h. Different superscripts indicate significant differences (p<0.05) amongst normoxic and hypoxic groups at different times. Values are expressed as mean ± SEM (n = 10).</p

p53 and Caspase-3 assay of embryonic cell under normoxia and hypoxia.

<p>(A). p<i>53</i>: p<i>53</i> expression was highest (<i>p</i><0.05) during 7 hpf, Beyond 24 h, p53 did not show any expression. p53 expression was not detected in normoxic embryos,. (B). Caspase 3: Caspase-3 showed significantly higher (p<0.05) expression in early stages during 2 hpf (cleavage stage) in hypoxia exposed embryos compared to control (normoxia). Different superscripts indicate significant differences (<i>p</i><0.05) amongst hypoxic and normoxic groups at different times. Values are expressed as mean ± SEM (n = 10).</p

Embryonic development of Goldfish under normoxia and hypoxia.

<p>(A) Embryos at 0.75 hpf (normoxia) showing blastodisc with four blastomeres, after appearance of the second cleavage furrow (vertical meridional) under hypoxia showing delayed 4 cell stage compared to the normoxia counterpart. (B). Embryos at 2 hpf: Embryos (normoxia) showing normal blastoderm with a composed mass of relatively small but distinct cells: under hypoxia showing delayed 64 celled stage, compared to the normoxia counterpart. (C). Embryos at 4 hpf: Epiboly stage arrived in normoxic embryos showing multicellular blastoderm, margin of which extends slightly over yolk. (D). Embryos at 7 hpf: Epiboly stage was delayed by 3 hours in hypoxic embryos. (E). Embryos at 12 hpf: Appearance of shield stage in normoxic embryos showing its visible axis with a narrow, transparent ridge, extending forward from the blastopore, encircling the yolk. The same was not observed in hypoxic counterparts. (F). Embryos at 24 hpf: Normoxic embryos showing somite stage whereas hypoxic embryos reaching shield stage within the same time, signifying delayed development by approximately 16 hrs. Scale: 200 µm.</p