In chitin-amended microcosms, these toxicant/substrate biotransformation rates were
higher across the salinity gradient, particularly at higher salinities, for all three toxicants.
Values for PH increased to 2.08 % h 1- ± 0.04 at 0 ppt and 1.875 ±0.07 %h -1 at 24 ppt. The
most significant rate increase was at 20 ppt. Methyl parathion chitin-amended biotransformation rates increased slightly to 1 .83 ± 0.11 % h -1 at 0 ppt and to l .60 ± 0.12 % h -1 at
24 ppt, a 26 % increase in toxicant biotransformation. PCP values were highly significant
at 0 ppt exhibiting a biotransformation rate of 0.66 ± 0.14% h -1 . This is roughly twice as
rapid a turnover of PCP than in non-amended microcosms. At higher salinities, PCP
biotransformation rate changes were equally significant, 0.26 ± 0.08% h -1 , demonstrating toxicant turnover, in the presence of chitin. In non-amended microcosms, biotransformation was not rated. Interestingly, this k value for PCP at 24 ppt was equal to
non-amended k value for PCP at 0 ppt.
In Figure 2, noticeable increases in toxicant biotransformation rates for chitin-amended
microcosms over non-amended was seen for both 2,4 dichlorophenol (2,4 DPH) and
l,2 dichloroethane (1,2 DE) for salinity levels shown. Values for 2,4 DPH ranged from
2,04 ± 0.16 % h -1 at 0 ppt to 1.65 ± 0.19% h -1 at 24 ppt for chitin-amended microcosms.
This compared with k values of 1.58 ±0.12% h -1 in non-amended microcosms for 0 ppt
and 24 ppt, respectively. The rate increase at 24 ppt for 2,4 DPH was highly significant.
Values for 1,2 DE were quite similar with the most significant increases in k noted for
chitin-amended saline microcosms. At 24 ppt, k values increased from 0.23 ± 0.04 % h -1
to 0.885 ± 0.10% h -1 .
Figure 2 also shows toxicant/substrate biotransformation profiles for Kepone (KP), an
organochlorine. Turnover of KP was not detectable for all non-amended microcosms.
For chitin-amended microcosms, only a slight biotransformation of KP was noted,
k = 0.008 ± 0.0004 % h -1 . This is approximately a 0.2 % removal rate of K P per day or
T 1/2 = 262 days. Subsequent radiotracer studies with
14 C-UL-Kepone (Portier and
Meyers, 1984) genereated values of 266 d for non-amended and 272 d for chitin amended
microcosms.
Toxicant Effects on Substrate Colonization
As shown earlier in Figures 1 and 2, significant changes in toxicant biotransformation
was noted for several toxicants in the presence of chitin. In subsequent microcosm
investigations using a radiolabelled chitin polymer unit, N-acetyl-D-glucosamine (glucosamine
14 C), toxicant effects on substrate biodegradation was examined. Manuscript
limitations prevent presentation of mineralization profiles for all toxicants for each
salinity range. Figure 3 presents information on
14 C-NAG mineralization in the presence
of 2,4 DPH and 1,2 DCE in saline microcosms at 24 ppt. These two toxicants, however,
exhibited the greatest increases in toxicant biotransformation. Total chitinoclasts, based
on colony forming units CFU/mL, were used to follow microbial population dynamics.
The toxicant 2,4 DPH had no significant effect on the chitinoclastic population with
levels of CFU/ml similar to control microcosms. However, at 12 h, CFU levels were
somewhat higher in 2,4 DPH microcosms. In 1,2 DCE microcosms, total chitinoclasts
were reduced through 12 h, with increases above initial CFU levels noted at 24 h. The
toxicant 1,2 DCE induced an incubation period of about 8 h to 12 h. Analysis of 14 CO2
expiration data confirmed this delay in NAG mineralization. A delay in substrate
turnover for 1-4 h was noted for 2,4 DPH. Thus, one could postulate that while chitin
addition significantly increased toxicant biotransformation over a time frame of days, at
the period of initial exposure, chitinoclastic populations are affected by the presence of
these toxicants.
583
higher across the salinity gradient, particularly at higher salinities, for all three toxicants.
Values for PH increased to 2.08 % h 1- ± 0.04 at 0 ppt and 1.875 ±0.07 %h -1 at 24 ppt. The
most significant rate increase was at 20 ppt. Methyl parathion chitin-amended biotransformation rates increased slightly to 1 .83 ± 0.11 % h -1 at 0 ppt and to l .60 ± 0.12 % h -1 at
24 ppt, a 26 % increase in toxicant biotransformation. PCP values were highly significant
at 0 ppt exhibiting a biotransformation rate of 0.66 ± 0.14% h -1 . This is roughly twice as
rapid a turnover of PCP than in non-amended microcosms. At higher salinities, PCP
biotransformation rate changes were equally significant, 0.26 ± 0.08% h -1 , demonstrating toxicant turnover, in the presence of chitin. In non-amended microcosms, biotransformation was not rated. Interestingly, this k value for PCP at 24 ppt was equal to
non-amended k value for PCP at 0 ppt.
In Figure 2, noticeable increases in toxicant biotransformation rates for chitin-amended
microcosms over non-amended was seen for both 2,4 dichlorophenol (2,4 DPH) and
l,2 dichloroethane (1,2 DE) for salinity levels shown. Values for 2,4 DPH ranged from
2,04 ± 0.16 % h -1 at 0 ppt to 1.65 ± 0.19% h -1 at 24 ppt for chitin-amended microcosms.
This compared with k values of 1.58 ±0.12% h -1 in non-amended microcosms for 0 ppt
and 24 ppt, respectively. The rate increase at 24 ppt for 2,4 DPH was highly significant.
Values for 1,2 DE were quite similar with the most significant increases in k noted for
chitin-amended saline microcosms. At 24 ppt, k values increased from 0.23 ± 0.04 % h -1
to 0.885 ± 0.10% h -1 .
Figure 2 also shows toxicant/substrate biotransformation profiles for Kepone (KP), an
organochlorine. Turnover of KP was not detectable for all non-amended microcosms.
For chitin-amended microcosms, only a slight biotransformation of KP was noted,
k = 0.008 ± 0.0004 % h -1 . This is approximately a 0.2 % removal rate of K P per day or
T 1/2 = 262 days. Subsequent radiotracer studies with
14 C-UL-Kepone (Portier and
Meyers, 1984) genereated values of 266 d for non-amended and 272 d for chitin amended
microcosms.
Toxicant Effects on Substrate Colonization
As shown earlier in Figures 1 and 2, significant changes in toxicant biotransformation
was noted for several toxicants in the presence of chitin. In subsequent microcosm
investigations using a radiolabelled chitin polymer unit, N-acetyl-D-glucosamine (glucosamine
14 C), toxicant effects on substrate biodegradation was examined. Manuscript
limitations prevent presentation of mineralization profiles for all toxicants for each
salinity range. Figure 3 presents information on
14 C-NAG mineralization in the presence
of 2,4 DPH and 1,2 DCE in saline microcosms at 24 ppt. These two toxicants, however,
exhibited the greatest increases in toxicant biotransformation. Total chitinoclasts, based
on colony forming units CFU/mL, were used to follow microbial population dynamics.
The toxicant 2,4 DPH had no significant effect on the chitinoclastic population with
levels of CFU/ml similar to control microcosms. However, at 12 h, CFU levels were
somewhat higher in 2,4 DPH microcosms. In 1,2 DCE microcosms, total chitinoclasts
were reduced through 12 h, with increases above initial CFU levels noted at 24 h. The
toxicant 1,2 DCE induced an incubation period of about 8 h to 12 h. Analysis of 14 CO2
expiration data confirmed this delay in NAG mineralization. A delay in substrate
turnover for 1-4 h was noted for 2,4 DPH. Thus, one could postulate that while chitin
addition significantly increased toxicant biotransformation over a time frame of days, at
the period of initial exposure, chitinoclastic populations are affected by the presence of
these toxicants.
583