Page 776 - Veterinary Toxicology, Basic and Clinical Principles, 3rd Edition

Aquatic Toxicology Chapter | 54 735

VetBooks.ir Benli et al. (2008) exposed Nile tilapia (Oreochromis which further decreases the affinity of Hb for oxygen.
Decreased oxygen tensions increase anaerobic metabolism
niloticus) to 0.0, 1.0, 2.0, 5.0 and 10.0 mg TA-N/1 of
and acidosis occurs. Exposure of rainbow trout to 1 mmol
ambient water for 6 weeks. Fish exposed to elevated TA-
N had a dose response increase in severity of histopatho- NO 2 causes vasodilation and an increased cardiac work-
2
logic lesions in the gills consisting of hyperemia, chloride load (Aggergaard and Jensen, 2001; Jensen and Agnisola,
cell proliferation, fusion of the secondary lamellae, and 2005). The fish died when the metHg was greater than
2
telangiectasis. Cloudy swelling and hydropic degenera- 70%. Plasma NO level was 2.9 mmol at the time of
2
tion were observed in the liver, and hyperemia and death. Liver cell damage linked to mitochondrial pathology
glomerulonephritis were observed in the kidney. Skin occurs, and hepatic stores of glycogen are depleted.
lesions were not observed. Elevated TA-N reduces Necrosis of the retina can occur. Under in vitro conditions,
2
growth in fish. Thyroid dysfunction has been observed in hepatocytes from rainbow trout detoxify NO by convert-
2
fish exposed to high ambient concentrations of NH 3 ,and ing NO 2 to considerably less toxic NO 2 (Doblander and
2 3
reduced expression of thyroid hormone receptor β and Lackner, 1996; Jensen and Hansen, 2011). Recovery from
insulin-like growth factor 1 (Sinha et al., 2012; Nugegoda nitrite poisoning appears to take several weeks, and com-
and Kibria, 2016). pensatory weight gain may or may not occur. There is a
2
spectrum of species susceptibility to NO , which is linked
2
2
2
Nitrite (NO ) to Cl uptake by the gills (Durborow et al., 1997; Jensen,
2 2003). Largemouth (Micropterus salmoides) and small-
Ammonium is oxidized to nitrate in a two-step process mouth bass (Micropterus dolomieu), bluegill (Lepomis
2
2
1
(from NH to NO to NO ) by aerobic bacteria. Aquatic macrochirus), and green sunfish (Lepomis cyanellus)are
4 2 3
2
animals, especially freshwater fish and crustacea, are relatively resistant to high concentrations of NO . Catfish
2
2
more at risk for NO poisoning than are terrestrial organ- (order Siluriformes), goldfish (Carassius auratus), fathead
2
isms (Camargo et al., 2005). Nitrite intoxication of minnows (Pimephales promelas), and tilapia (genus
2
aquatic animals occurs when conditions exist for imbal- Tilapia) are sensitive to NO , and cold-water fish such as
2
2
ance in the nitrogen cycle. Freshwater fish are more sus- rainbow trout are highly sensitive to NO . Nitrite poison-
2
ceptible to NO 2 than are saltwater fish. In freshwater ing can be prevented by adding Cl 2 to the water
2
2
fish, NO is rapidly absorbed across the gills. The gener- (Durborow et al., 1997). The most common option is to
2 2 2
2
ally accepted mechanism for NO absorption is by com- add Cl to the water to achieve a 10:1 ratio of Cl to
2
2 2
peting for chloride ion (Cl ) uptake across the gills. NO . Decreased feeding rates and increased throughput of
2
2
Chloride ion is exchanged for bicarbonate (HCO ), and nonrecycled water are alternative methods of controlling
3 2
this exchange occurs in the apical part of the gill epithe- NO . Bacterial and parasitic disease increases the sensitiv-
2
2 2 2
lial cell. Nitrite has affinity for the Cl /HCO exchange ity of fish to NO poisoning. The presence of concurrent
2
3
2
protein and replaces Cl in the exchange process. infectious disease requires increasing the concentration of
2 2
Increasing the water concentration of Cl reduces the tox- ambient Cl . Catfish producers commonly maintain
2
2
icity of NO . Fish with high Cl uptake, such as rainbow 100 ppm Cl 2 in the pond or tank water as insurance
2
trout, perch (family Percidae), and northern pike (Esox against an increase in NO 2 levels or to counteract the
2
2 2
lucius), are more susceptible to NO . Millimolar NO 2 effects of concurrent infectious disease. Dietary vitamin E
2
2
levels in such fish, especially if Cl in the water is low, may also be protective against nitrite poisoning.
2
can result from micromolar levels of NO exposure from
2
2
water. Nitrite causes a net loss of Cl because there is a
2
2
reduction in the influx of Cl , and it stimulates a net loss Nitrate (NO )
1
of K from muscle, causing an extracellular hyperkalemia 3
2
1
and increased excretion of K . Nitrite also enters red Fish, comparing NH 3 and NO , are relatively resistant to
2
2
blood cells and oxidizes Fe 12 (ferrous) in hemoglobin NO intoxication. Nitrate accumulation can be .100 mg
3
2
(Hb) to Fe 13 (ferric), forming methemoglobin (metHb) NO /L of water. Nitrate poisoning is commonly associ-
3
(Grabda et al., 1974). The blood becomes discolored ated with accidental increases caused by nitrate rich run-
brown, a characteristic diagnostic feature of methemoglo- off water contaminating water sources. Larval forms of
binemia. The oxidation of Fe 12 to Fe 13 changes oxygen fish generally are the most sensitive life stages. Chronic
affinity of Hb and oxygen tensions in blood drop toward NO 2 poisoning in rainbow trout was studied using
3
2
dissolved oxygen in ambient water. Changes in oxygen 26.2 ppm NO 3 and a static tank system (Grabda et al.,
affinity and blood pH increase movement of oxygen 1974). Fish were observed to gather around the aeration
to the swim bladder, thus affecting buoyancy. In system. Liver pathology consisting of degenerative
2
teleost (bony) fish, there is NO -mediated disruption of changes and necrosis was observed, and degenerative
2
1 1
the Na /H exchange mechanism in the red blood cell, changes were observed in the hemopoietic centers.