7091

• UCREFRP Catalog Number: 7091
• Author: Eisler, R.
• Title: Tin Hazards to Fish, Wildlife, and Invertebrates
• USFW Year: 1989.
• USFW - Doc Type: A Synoptic Review.
• Copyright Material: NO

In any member of the organotin series R SnX progressive substitution
of organic groups at tin produces a maximuM Po o'gical activity for the
triorganotin derivatives, R SnX (Davies and Smith 1982). Among triorganotin
compounds, trimethyltins are Highly toxic to insects, birds, and mammals;
triethyltins to mammals; tripropyltins to gram-negative bacteria; tributyltins
to fish, molluscs, fungi, and gram-positive bacteria; triphenyltins to fish,
fungi, and molluscs; and tricyclohexyltins to mites (Duncan 1980; Davies and
Smith 1982; Maguire et al. 1982; Blunden and Chapman 1986). In mammals, the
lower triorganotin homologues (trimethyltins, triethyltins) are essentially
neurotoxic, the intermediate trialkyltins and triphenyltins are primarily
immunotoxic, and the higher homologues are only slightly toxic or not toxic
(Krigman and Silverman 1984; Snoeij et al. 1985). The toxicity of
triorganotin compounds is probably due to their ability to bind to proteins
and to inhibit mitochondrial oxidative phosphorylation (Smith 1978b; Duncan
1980; WHO 1980; Davies and Smith 1982; Blunden and Chapman 1986).
Triorganotins also interfere with phagocytosis and exocytosis and other
pathways where sulfhydryl groups play a pivotal role (Elfe?ink et al. 1986),
and inhibit uptake of gamma-aminobutyric acid and Na -K -ATPase in brain
(Costa 1985). Impairment of phagocytosis and related activities of
polymorphonuclear leukocytes may enhance susceptibility for infection
(Elferink et al. 1986).
Trimethyltins are the most toxic trialkyltins to mammals, regardless of
the nature of the substituent (X group) according to Smith (1978b). They
induce pathological lesions in brain and overt neurological and behavioral
changes in rodents (Chang 1986). Trimethyltins are neurotoxins that damage the
limbic system, cerebral cortex, and brain stem and can traverse the placenta
and accumulate in the fetus (Reuhl and Cranmer 1984). Trimethyltins (but not
inorganic, monomethyl, or dimethyl?ins) inhibit brain protein synthesis by 47%
and can cause a decrease of 4.2 C in body temperature of mice within 1 hour
postadministration of 3.0 mg/kg bodg weight (Costa and Sulaiman 1986).
Raising the ambient temperature to 35 C prevented hypothermia in treated mice
and resulted in only a 20% inhibition in protein synthesis. More research is
needed on the role of protein synthesis in organotin-induced neurotoxicity.
Triethyltins modify phosphorylation processes in subcellular fractions of
rat brain proteins (Piver 1973; Neumann and Taketa 1987). Signs of
triethyltin poisoning in rodents include weakness of hindlimbs, dyspnea, and
peripheral vasodilation (Watanabe 1980). Internally, acute triethyltin
intoxication is characterized by a transient edema of the central and
peripheral nervous systems manifested by extensive intramyelinic vacuolation
due to splitting of myelin lamellae; changes are reversible (Watanabe 1980;
Reuhl and Cranmer 1984). Neuronal death is reported following triethyltin
intoxication during the neonatal period, possibly as a result of elevated
intracranial pressure (Reuhl and Cranmer 1984). In rabbit brain, triethyltins
alter activity of pyruvate dehydrogenase (Neumann and Taketa 1987).
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